Category Archives: Evolution

Berry Go Round #49 – all the plants fit to print

Welcome to the newest edition of Berry Go Round, a blog carnival devoted to highlighting recent blog posts about any and every aspect of plant life. This is the third time I am hosting BRG (see #7 and #31) which is not so bad for a zoologist 😉

There is not much more I can add, and the entries this month are wonderful, so instead of wasting your time with my own musings, let’s dig into the carnival itself!

21stcenturynaturalist at the 21stcenturynaturalist: Alien Legacy of the Building Boom in Ireland:

This unseasonably warm winter has seen the blossoming of crocuses, daffodils and snowdrops in gardens throughout Ireland a lot earlier than usual. It makes a change from the previous two years, when this blog noted that daffodils had yet to bloom by March…

Hollis at In the Company of Plants and Rocks: Leaving Home:

Isn’t it interesting that many humans have a hard time letting their children go, while most animals and plants take the opposite approach — rebuffing, excluding and even hurling their progeny into the unknown…

Elizabeth Preston at Inkfish: Seeds from 30,000-Year-Old Squirrel Cache Flower Again:

Confession: As a nerdlet of nine or ten, I decided to help flowers get fertilized. I loved seeing the glossy seeds hidden inside the fat green ovaries of dead flowers when I split them open with my thumbnail. I must have watched one of those nature specials where the scientists climb up to the top of the Alps and dust pollen onto endangered flowers with a paintbrush, because I started going around roadside fields with cotton balls and gathering pollen. Partway through my project I realized that these particular plants were doing fine without human intervention, and abandoned them…

Ed Yong at Not Exactly Rocket Science: Flowers regenerated from 30,000-year-old frozen fruits, buried by ancient squirrels:

Fruits in my fruit bowl tend to rot into a mulchy mess after a couple of weeks. Fruits that are chilled in permanent Siberian ice fare rather better. After more than 30,000 years, and some care from Russian scientists, some ancient fruits have produced this delicate white flower…

Jason G. Goldman at The Thoughtful Animal: Are Sheep Better at Botany than the US Government?:

Botanically, a tomato is a fruit: a seed-bearing structure that grows from the flowering part of a plant. In 1893, however, the highest court in the land ruled in the case of Nix v. Hedden that the tomato was a vegetable, subject to vegetable import tariffs. Unfortunately, the vegetal confusion did not end in 1893. Indeed, confusion over botanical categorization has a proud history in America. Just recently, the US Congress mistook pizza (or, specifically, the tomato paste found on what passes for pizza in school lunchrooms) for a vegetable! And a Fox News anchor apparently had trouble distinguishing between peppers and military-grade pepper spray.

Sheep can do better…

Laura Baker at Save Knowland Park: The Rare Chaparral Plant Community of Knowland Park:

There are several different types of native shrub communities in Knowland Park, but none is as rare or fascinating as the remnant stand of maritime chaparral located on the northwestern side of the park. Chaparral is a quintessential California vegetation, and winter is an excellent time of year to explore the chaparral at Knowland Park. As you follow the path into brush, you’ll find yourself in a maze-like realm of twisted, lichen-encrusted trunks and unique plant life. Truly wondrous!…

Chris Clarke at The Back Forty: How to Appreciate Old-Growth Desert:

The desert has secrets, and it doesn’t give them up freely. This patch of Low Desert I’m camped on east of Joshua Tree National Park seems a quiet bit of desolation, a few scraggly shrubs separated widely with non-descript gravel between them. A few aging beer cans, a few tracks across the landscape left by off-road vehicles. The surroundings mostly seem to contain wind, and cold sun, and silence. Not much to write home about, a person might think.

That person would be wrong…

Karl Haro von Mogel at Biofortified: How to pollinate Carrots and Beets:

Ladies and gentlemen, here is the latest in my series of Pollination Methods videos that I make as part of my thesis project. While carrots and beets are not closely related, they share similar life cycles, pollination methods, and even breeding goals – so I put both of these root vegetables in the same video…

Ian Lunt at Ian Lunt’s Ecological Research Site: There goes the neighborhood:

Every now and then I stumble across a graph in a paper that blows me away. Some show patterns I hadn’t imagined, while others show patterns far stronger than I’d thought possible. The other day I came across an ‘in your face’ graph that’s worth sharing…

Luigi at Agricultural Biodiversity Weblog: Looking for a (double) grain in a seedbank:

The fact that IRGC 59101 (which is pictured below, thanks to Ms de Guzman again) is a bit of a strange morphological variant isn’t mentioned in the genebank database, however. Not the electronic version, anyway. Ms de Guzman simply remembered the variety and dove back into her notebooks to find it. Next time I think about venturing into Genebank Database Hell, I want her as my guide…

The Phytophactor at The Phytophactor: More unnatural blueness!:

Blueness is coming out of the floral woodwork, or out of the dye bottle actually, which is clearly a crime against nature…

Colin Beale at Nothing in biology makes sense!: The paradox of the prickly: Why grow thorns if they don’t work?:

Spinescent. Now there’s a word! It simply means having spines and one of the first things many visitors to the African savannah notice is that everything is covered in thorns. Or, in other words, Africa is spinescent. It’s not a wise idea to brush past a bush when you’re walking, and you certainly want to keep arms and legs inside a car through narrow tracks. These are thorns that puncture heavy-duty car tyres, let alone delicate skin. But why is the savanna so much thornier than many of the places visitors come from? Or even than other biomes within Africa, such as the forests?…

Colin Beale at Safari Ecology: Myrrh trees (Commiphora) are useful things… :

Having last week given you the bad news about the biological warfare that plants with thorns are engaging in, I thought it only fair to share some tips that may help you stave off those tropical nasties threatening to kill you… So the good news is that some of those very same thorny trees that are out to get you also hold the cure in their sap…

Jes at Biogeography Bits: Floral gladiators evolve faster in South Africa than Rome:

Gladiolus is latin for ‘little sword’, a fitting name for a plant whose flowers grow along giant spikes. While these plants are ubiquitous in gardens across the United States, they actually are complete foreigners. Of the 260 species around the world, almost all are from southern Africa, and none are from North or South America…

Roberta at Growing With Science Blog: Seed of the Week: Giraffe Thorn Acacia:

Our seeds from last week were tough to identify, but thank you to everyone who sent guesses. I appreciate your attempts because they give me great ideas for upcoming mystery seed posts 🙂 The mystery seeds were from a giraffe thorn tree, Acacia erioloba. It is also commonly called camel thorn…

Colin Beale at Safari Ecology: Commelina, the Maasai Reconciliation Grass:

It’s surprisingly easy these days to find information on the medicinal use of plants (there’s a great list for the Samuru people here, for example), such as the Commiphora uses we covered last week, but many plants have cultural significance beyond the simple medicinal uses and it’s often much harder to find information about these uses…

Sally at Foothills Fancies: The Blue Rabbitbrush Road

How native is native? We have to applaud the trend toward using more native species in efforts to reclaim natural landscapes after disturbance, don’t we? Sometimes, unfortunately, the gesture backfires no matter how well intentioned it may be. Such was the case several years ago (about 2006?), when the Town of Morrison built a water pipeline through the local open space park (Mt. Falcon)…

David Bressan at History of Geology: How Plants survived the Ice Age:

There are various methods to reconstruct the plant community of a past landscape. Flowering plants produce pollen grains composed by a chemically very stable substance named Sporopollenin, therefore pollen grains usually are well preserved in sediments (but as correctly noted in the comments not in soils). Identifying and counting the pollen deposited over time on the bottom of a lake or conserved in the layers of a bog we can infer the vegetation that once surrounded these sediment traps. In such sediments also plant detritus can be conserved…

Ryan D. Kitko at Cunabulum: The orchid that smells like Chanel No 5:

The orchid genus Dipodium, collectively known as the hyacinth orchids, includes somewhere between 20 to 30 species native to Southeast Asia and Australia. Interestingly, the majority of the species are leafy epiphytes – well, terrestrials that climb and then become epiphytes – dispersed throughout Southeast Asia. A small group of these plants, however, have lost the leaves entirely and live as terrestrial parasites at the base of Eucalyptus trees in Australia…

Andrea Wills at A bouquet from Mendel: Why “Natural” isn’t always better: almond extract and cyanide:

Right now the various species of Prunus are in flower all over northern California; the ornamental plums that are so popular as sidewalk decor are shedding petals everywhere, apricot blossoms are peeking out from yards, and the almond trees that crop up as renegades from the big orchards near Davis and in the central valley are covered in popcorn-y pinkish white flowers. With constant reminders of stone fruit everywhere but none actually in season to eat, I’ve been doing a lot of baking with almonds and almond extract…

S.E. Gould at Lab Rat: Plants that shut out bacterial invaders:

I have a soft-spot for plant biology. In my final year at university, having exhausted all of the bacteria-related biochemistry lectures, I took a bacteria-related lecture course with the plants department. It was a smaller department, and seemed a lot friendlier and nicer. Also the biscuits in the tea-room were cheaper. So I do like to write about plants every now and again, and it isn’t a very difficult task because like every other multicellular organism on the planet, plants also suffer from bacterial infections. Unlike humans, they don’t have a blood stream to carry immune cells around, so they instead rely on bombarding bacteria with nasty chemicals, quickly killing off any parts of the plant that get infected and acquiring a kind of plant resistance to stop attacks occurring again…

With that, we conclude this month’s edition of Berry Go Round. Next month’s carnival will be hosted by Greg Laden. Send in your submissions and volunteer to host.

Clocks in Bacteria II: Adaptive Function of Clocks in Cyanobacteria

This is the second post in a series of five, originally published on April 05, 2006:

In the previous two posts, here and here, I have mentioned how the discovery of circadian clocks in Cyanobacteria changed the way we think about the origin and evolution of circadian clocks. Quite soon after the initial discovery, the team from Carl Johnson’s laboratory published two papers [1,2] describing a more direct test of adaptive function of circadian clocks in the Synechococcus elongatus.

Wild-type and various clock-mutants in Synechoccocus, when raised in isolation in light-dark cycles, have comparable reproductive rates. When raised in constant light, they fare even a little better, i.e., multiply faster. Thus, in isolation, clock does not appear to confer adaptive advantage.

However, when the strains are cultured together, two strains grown in the same petri-dish, and exposed to light-dark cycle, the strain whose endogenous period is closer to the period of the environmental cycle “wins” the contest. This suggests that circadian clock confers fitness in rhythmic environments. In constant light, arrhythmic mutants outperform rhythmic strains.

Here is how Johnson describes the experiments (from a book chapter not available online):

“The authors’ laboratory tested the adaptive significance of circadian programs by using competition experiments between different strains of the cyanobacterium Synechococcus elongatus (Ouyang et al., 1998; Woelfle et al., 2004). For asexual microbes such as S. elongatus, differential growth of one strain under competition with other strains is a good measure of reproductive fitness. In pure culture, because the strains grew at about the same rate in constant light and in LD cycles, there did not appear to be a significant advantage or disadvantage in having different circadian periods when the strains were grown individually. The fitness test was to mix different strains together and to grow them in competition to determine whether the composition of the population changes as a function of time. The cultures were diluted at intervals to allow growth to continue. Different period mutants were used to answer the question, ”Does having a period that is similar to the period of the environmental cycle enhance fitness?” The circadian phenotypes of the strains used had freerunning periods of about 22 h (B22a, C22a) and 30 h (A30a, C28a). These strains were determined by point mutations in three different clock genes: kaiA (A30a), kaiB (B22a), and kaiC (C22a, C28a). Wild type has a period of about 25 h under these conditions. When each of the strains was mixed with another strain and grown together in competition, a pattern emerged that depended on the frequency of the LD cycle and the circadian period. When grown on a 22-h cycle (LD 11:11), the 22 h-period mutants could overtake wild type in the mixed cultures. On a 30-h cycle (LD 15:15), the 30 h-period mutants could defeat either wild type or the 22 h-period mutants. On a ”normal” 24-h cycle (LD 12:12), the wild-type strain could overgrow either mutant (Ouyang et al., 1998). Note that over many cycles, each of these LD conditions have equal amounts of light and dark (which is important, as photosynthetic cyanobacteria derive their energy from light); it is only the frequency of light versus dark that differs among the LD cycles. Figure 1 shows results from the competition between wild type and the mutant strains (Ouyang et al., 1998).
Clearly, the strain whose period most closely matched that of the LD cycle eliminated the competitor. Under a nonselective condition (in this case, constant light), each strain was able to maintain itself in the mixed cultures. Because the mutant strains could defeat the wild-type strain in LD cycles in which the periods are similar to their endogenous periods, the differential effects that were observed are likely to result from the differences in the circadian clock. A genetic test was also performed to demonstrate that the clock gene mutation was specifically responsible for the differential effects in the competition experiment (Ouyang et al., 1998). Because the growth rate of the various cyanobacterial strains in pure culture is not detectably different, these results are most likely an example of ”soft selection” where the reduced fitness of one genotype is seen only under competition (Futuyma, 1998).
In a test of the extrinsic versus intrinsic value of the clock system of cyanobacteria, wild type was competed with an apparently arrhythmic strain (CLAb). As shown in Fig. 2, the arrhythmic strain was defeated rapidly by wild type in LD 12:12, but under competition in constant light, the arrhythmic strain grew slightly better than wild type (Woelfle et al., 2004). Taken together, results show that an intact clock system whose freerunning period is consonant with the environment significantly enhances the reproductive fitness of cyanobacteria in rhythmic environments; however, this same clock system provides no adaptive advantage in constant environments and may even be slightly detrimental to this organism. Therefore, the clock system does not appear to confer an intrinsic value for cyanobacteria in constant conditions.”

It is telling how many control experiments they had to do in order to eliminate various alternative explanations. They had to show that mutations in clock genes do not have additional effects on the ability of the cell to grow and reproduce. Check. They had to show that clock mutations do not affect the ability of the cells to utilize the food and light energy. Check. They had to show that clock mutations do not affect any conceivable way by which one strain can, perhaps by secreting chemicals, actively disrupt the health of the other strain. Check. And in the end, although they demonstrated that “resonance”, i.e., similarity between environmental cycle and the intrinsic period confers some advantage, they still could not state with certainty that this “proves” that the circadian clock has an adaptive function.

Here is Johnson [3] again:

“The original adaptation of circadian clocks was presumably to enhance reproductive fitness in natural environments, which are cyclic (24h) conditions. We can refer to this situation as an adaptation to extrinsic conditions. However, some researchers have proposed that circadian clocks may additionally provide an “intrinsic” adaptive value (Klarsfeld 1998; Paranjpe 2003 and Pittendrigh 1993). That is, circadian pacemakers may have evolved to become an intrinsic part of internal temporal organization and, as such, may have become intertwined with other traits that influence reproductive fitness in addition to their original role for adaptation to environmental cycles. Note that a rigorous evolutionary biologist would no longer consider an intrinsic value for clocks to be an adaptation if their original extrinsic value has been lost. However, if clocks retain extrinsic value and additionally accrue intrinsic value, then they would still be considered an adaptation.”

Testing if a trait is an adaptation is a very difficult task. Testing if something as ubiquitous as a circadian clock is an adaptation is even harder. Can you imagine testing if using ATP for energy storage, or using DNA for information storage are adaptations? Are there organisms that do not use these, so we can use them in comparative or competitive studies?

In his book Adaptation and Environment (1990), Robert Brandon came up with five criteria that need to be satisfied in order to determine if a trait is an adaptation (thanks to Robert Skipper for a reminder of this):

“One must have
1. evidence that selection has occurred;
2. an ecological explanation of the fact that some types are better adapted than others;
3. evidence that the trait in question is heritable;
4. information about the structure of the population, including both demic structure and the structure of the selective environment;
5. phylogenetic information concerning what has evolved from what.”

The early cyanobacterial studies have shown criterion #3 to be correct. The competitive assay studies started cracking the criterion #2. In the next post on this topic, I will describe some studies that started investigating the criterion #5, with some additional evidence for criteria Nos. 1, 2 and 4. Apparently, we still have a long way to go. Johnson again:

An example from the circadian literature of a ”just-so” story that the author has personally promulgated is that of ”temporal separation” of photosynthesis and nitrogen fixation in cyanobacteria. In nitrogen-fixing unicellular bacteria, nitrogen fixation is often phased to occur at night. Nitrogen (N2) fixation is inhibited by low levels of oxygen, which poses a dilemma for photosynthetic bacteria because photosynthesis generates oxygen. Mitsui et al. (1986) proposed that the nocturnal phasing of nitrogen fixation was an adaptation to permit N2 fixation to occur when photosynthesis was not evolving oxygen, and the author has repeated this hypothesis in several publications (Johnson et al., 1996, 1998). This hypothesis would predict that cyanobacterial growth in constant light would be slower than in a light/dark (LD) cycle because nitrogen fixation would be inhibited under these conditions and therefore the growing cells might rapidly become starved for metabolically available nitrogen. The problem is that cyanobacteria grow perfectly well in constant light–in fact, they grow faster in constant light than in LD cycles, presumably because of the extra energy they derive from the additional photosynthesis. This result is inconsistent with the ”temporal separation” hypothesis. It does not mean that the ”temporal separation” hypothesis is incorrect–in fact, the author believes that under appropriate (but as yet untested) conditions of medium, light, and carbon dioxide, the ”temporal separation” hypothesis will emerge triumphant. Nevertheless, the point here is that ”temporal separation in cyanobacteria” is an example of a ”just-so” circadian story that we like to tell without its being rigorously supported by appropriate data. This was the conclusion of Gould and Lewontin (1979) for many investigations in the field of population biology, and this criticism is on target.”

References and image sources:

[1] YAN OUYANG, CAROL R. ANDERSSON, TAKAO KONDO, SUSAN S. GOLDEN, AND CARL HIRSCHIE JOHNSON, Resonating circadian clocks enhance fitness in cyanobacteria, Proc. Natl. Acad. Sci. USA, Vol. 95, pp. 8660-8664, July 1998

[2] Mark A. Woelfle, Yan Ouyang, Kittiporn Phanvijhitsiri and Carl Hirschie Johnson, The Adaptive Value of Circadian Clocks: An Experimental Assessment in Cyanobacteria, Current Biology, Vol. 14, 1481-1486, August 24, 2004,

[3] Carl Hirschie Johnson, Testing the Adaptive Value of Circadian Systems, Methods in Enzymology, Volume 393 , 2005, Pages 818-837

Clocks in Bacteria I: Synechococcus elongatus

From the Archives: first in a series of five posts on clocks in bacteria first published on March 08, 2006.

As I stated in the introductory post on this topic, it was thought for a long time that Prokaryotes were incapable of generating circadian rhythms. When it was discovered, in 1994 [1], that one group of Prokaryotes, the cyanobacteria, possess a circadian clock, the news was greeted with great excitement. This was the first definitive demonstration of a circadian clock in a bacterium (I intend to revisit the E.coli saga in a later post).

Synechococcus

All three hypotheses for the origin of the circadian clock suppose that it first evolved in an aquatic, unicellular organism. While protists fit the bill quite nicely, having a bacterium with a circadian clock pushed the origin of the clock further back into the past. This made the researchers happy as it supported the notion that the clock was a universal property of life, as well as that it evolved only once in the history of Life on Earth. This also suggested that clocks in all organisms use same or similar intercellular mechanisms for generation of circadian rhythms.

At the time that clocks were discovered in cyanobacteria, only two circadian genes were characterized: period in fruitflies and frequency in Neurospora crassa. The second fly gene, timeless, was discovered the following year, and the first mammalian gene Clock and the first plant gene Toc were discovered some years later. Thus, at the time, it was still plausible that all of life used the same mechanism for the circadian clock, just as all of life uses ATP for energy storage and DNA for information storage.

However, studying genetics in bacteria is a much quicker and easier task than in the large multicellular eukaryotes. Very soon, the cyanobacterial clock genes were discovered and it turned out that they had no resemblance to fly or mold genes. KaiA, KaiB and KaiC (as they were discovered in Japan, they were named “kaiten”, which implies a cycle of events reminiscent of the turning of the heavens) have no homologies with any of the clock genes found in any other group of organisms and the internal logic of the bacterial clock is different from that in plants, fungi and animals, i.e., it is not a typical transcription-translation feedback loop.

Method for studying the cyanobacteria clock

The clock in cyanobacteria is better thought of as a relay switch. It turns about 2/3 of the genome on in the morning (and off in the evening) and turns on the remaining 1/3 of the genome at dusk (and off at dawn). Recent findings about bacterial, plant, protist, fungal and animal clocks suggests as many as five separate events of the origin of a circadian clock on Earth – one for each major group of organisms.

Mutations and deletions [1,2 5,6] of either one of the three Kai genes affect the circadian phenotype, either by altering the inherent period of the freerunning rhythm, or by abolishing rhythmicity altogether. Interestingly, Synechococcus cells appear to have a “memory” of the circadian phase in which they find themselves and this memory gets transmitted from parental to daughter cells during cell division.

Synechococcus rhythm

Actually, under certain conditions, cell division is a much more rapid process than a circadian cycle. In other words, Synechococcus may undergo several cell divisions over a period of a single day, yet the colony as a whole keeps its circadian rhythms running all along [2,3].

Next time, I will focus on the contributions of cyanobacteria to the understanding of the origin, evolution and adaptive function of circadian clocks.

~~~~~

References, sources of images, and further reading:

[1] Circadian clock mutants of cyanobacteria by Kondo T, Tsinoremas NF, Golden SS, Johnson CH, Kutsuna S, Ishiura M., Science.266(5188):1233-6 (1994, Nov 18)

[2] Circadian clocks in prokaryotes by Carl Hirschie Johnson, Susan S. Golden, Masahiro Ishiura & Takao Kondo, Molecular Microbiology, Volume 21 Page 5 (July 1996).

[3] Circadian Rhythms in Rapidly Dividing Cyanobacteria by Takao Kondo, Tetsuya Mori, Nadya V. Lebedeva, Setsuyuki Aoki, Masahiro Ishiura and Susan S. Golden, Science, Vol. 275. no. 5297, pp. 224 – 227 (10 January 1997)

[4] Independence of Circadian Timing from Cell Division in Cyanobacteria by Tetsuya Mori and Carl Hirschie Johnson, Journal of Bacteriology, p. 2439-2444, Vol. 183, No. 8 (April 2001)

[5] CYANOBACTERIAL CIRCADIAN CLOCKS — TIMING IS EVERYTHING by Susan S. Golden & Shannon R. Canales, Nature Reviews Microbiology 1, 191-199 (2003)

[6] Circadian rhythms: as time glows by in bacteria by Johnson CH, Nature 430, 23-24 (2004)

Circadian Clocks in Microorganisms

From the Archives: this is the first in a series of posts on circadian clocks in microorganisms , originally published on February 23, 2006

Many papers in chronobiology state that circadian clocks are ubiquitous. That has been a mantra since at least 1960. This suggests that most or all organisms on Earth possess biological clocks.

In the pioneering days of chronobiology, it was a common practice to go out in the woods and collect as many species as possible and document the existence of circadian rhythms. Technical limitations certainly influenced what kinds of organisms were usually tested.

Rhythms of locomotor activity are the easiest to measure. Rodents, as well as large walking insects like cockroaches, will turn running wheels, each revolution triggering a switch that sends a signal to the computer. Songbirds will jump from one perch to another, each perch flipping a switch connected to a computer. Lizards, while walking around the cage will tilt the cage from left to right around an axis – a metal bar on the bottom – which will turn a switch. Plants that exhibit leaf movements (closing at night, opening during the day) were the prime experimental models for a while (e.g., Kalanchoe, mimosa, tobacco).

Monitoring rhythms in other organisms is much harder: it is mighty difficult to make a fish run in a running wheel, or build hopping perches sensitive enough to be triggered by the landing of a butterfly. That was even harder back in the late 1940s and early 1950s when most of this work was done.

The tree of life.

It is no suprise that nobody looked at microorganisms back then – it was just technically too hard. The fact is that most of the pioneers in the field came in from vertebrate physiology, ethology or ecology. It is easy for us, large mammals, to forget that we are not among the dominant life-forms on the planet – that title goes to bacteria, in terms of numbers of individuals, in terms of biodiversity, and in terms of total biomass. See if you can find mammals, or even all animals on the Tree of Life:

Some old papers, mostly parts of Conference Proceedings of various kinds, mention as fact that Bacteria do not have clocks but do not provide any citations. It took me years to dig out three papers (Rogers and Greenbank, 1930, Halberg and Connor, 1961; and Sturtevant, 1973) with relevance to this question and all three are ambiguous about the final verdict. Why is nobody revisiting this with modern molecular techniques?

Being unicellular does not preclude one from having a clock, though, as single-cell Protista and Fungi all have circadian rhythms, which have been studied quite extensively since the 1970s or so (I intend to delve some more in that literature and write some posts on them in the future).

Cyanobacteria

One group of bacteria does have a clock – the unicellular Cyanobacteria (if you are above a certain age, you may remember them under their old name: blue-green algae), in particular those species that do not form chains, e.g., Synechococcus and Nostoc. This was discovered very recently – only ten years ago (Mori et al. 1996). I was two years into my Masters when that paper appeared and I remember the excitement. I will certainly write a post or two on those soon [Note: yes, those posts are written and will be republished here over the next few days].

There has not yet been a single study of any kind of rhythmicity in Archaea [Note: there has been since this post was first published]. Most of those microorganisms live in strange places – miles deep under the surface of the earth, in rocks, in ice, on the ocean floors and in the hydrothermal vents. They mostly do not inhabit rhythmic environments, so perhaps they do not need to have clocks – but it would be really nice to know if that is really the case.

Archaea

Old Faithful, the famous geyser in Yellowstone park contains Archea. As the geyser erupts every 45 minutes or so, the microbes are suddenly exposed to very different environment: light, turbulence, lower temperature. Should we expect them to evolve a 45-minute clock that will help them predict the eruption so they can limit some sensitive biochemical reactions to the quiet periods and switch on the defenses against light and cold every 45 minutes?

In The Geometry of Biological Time, Arthur T. Winfree suggested an experiment (on Page 580) that it

“… should be possible to demonstrate the effect by bacterial selection experiments in a chemostat. By alternating the nutrient influx from glucose without oxygen, to oxygen without glucose, to alanine and oxygen, cells would be forced into a three-point metabolic cycle.” and “… reversing the order of the driving cycle, it should be possible also to select cells whose clocks run backward.”

In a later edition (after we learned that cyanobacteria have clocks) he suggested, instead, to use

“one of the species of cyanobacteria that revealed no circadian rhythms in surveys before Mori et al. (1996), and use light as the alternative nutrient”.

E.coli

As of today, nobody has performed such an experiment, although Elowitz and Leibler (2000) came pretty close with a study in which they produced oscillations in Escherichia coli with periods of 3-4 hours, which are slower than the cell-division cycle:

So, if most of Life on Earth is Prokaryotic (Eubacteria and Archaea), and those groups do not have clocks, then clocks are not ubiqutous, are they? In my papers and in my Dissertation I try to hedge a bit by stating that they are found in “organisms that live on or close to the surface of the Earth”, thus at least avoiding the deep-oceanic, deep-soil, and parasitic microorganisms (as well as burrowing and cave organisms that may have secondarily lost their clock).

Carolus Linnaeus’s Floral Clocks

I originally published this post on May 23, 2007, on the day of the 300th birthday of Karl Linne.

When it’s someone’s birthday it is nice to give presents, or a flower. Perhaps a whole boquet of roses. But if the birthday is a really big round number, like 300, and the birthday boy is the one who actually gave names to many of those flowers, it gets a little tougher. Perhaps you may try to do something really difficult and build, actually plant, a Flower Clock. After all, it was Carl von Linne, aka Carolus Linnaeus, today’s birthday celebrator, who invented the flower clock. He drew it like this, but he never actully built one:

The first one to make (and write down) an observation that some plants (in that case, a tropical Tamarind tree) raise their leaves during the day and let them droop down during the night, was Androsthenes, an officer who accompanied Alexander the Great. In the first century, Pliny the Elder made a similar observation, repeated in the thirteenth century by Albertus Magnus.

In 1729, Jean Jacque d’Ortous de Mairan, an astronomer, not a botanist, reported an experiment – considered to be the first true chronobiologial experiment in history – in which he observed the spontaneous daily rise and nightly fall of leaves of Mimosa pudica kept in a closet in the dark. The experiment was repeated with some improvements by Duhamel de Monceau and by Zinn, both in 1759.

Another Swede, Arrhenius argued that a mysterious cosmic Factor X triggered the movements. Charles Darwin published an entire book on the Movement of Plants, arguing that the plant itself generates the daily rhythms. The most famous botanist of the 19th century, Pfeffer, started out favouring the “external hypothesis”, but Darwin’s experiments forced him to change his mind later in his career and accept the “internal” source of such rhythmic movements. In the early 20th century, Erwin Bunning was the first to really thoroughly study circadian rhythms in plants. For the rest of the century, animal research took over and though there has been some progress recently, the understanding of clocks in plants still lags behind that of Drosophila and the mouse.

But it was Carolus Linnaeus back in the 18th century who, fond of personifying plants (mostly in regard to sex) named this phenomenon “sleep” in plants. Soon, he switched his focus from movements of leaves to the daily opening and closing of flowers and performed a broad study of the times of day when each flower species opened and closed:

Linnaeus observed over a number of years that certain plants constantly opened and closed their flowers at particular times of the day, these times varying from species to species. Hence one could deduce the approximate time of day according to which species had opened or closed their flowers. Arranged in sequence of flowering over the day they constituted a kind of floral clock or horologium florae, as Linnaeus called it in his Philosophia Botanica (1751, pages 274-276). A detailed and extended account of this in English will be found in F.W.Oliver’s translation of Anton Kerner’s The Natural History of Plants, 1895, vol.2, pages 215-218. As many of the indicator plants are wildflowers and the opening/closing times depend on latitude, the complexities of planting a floral clock make it an impractical proposition.

While it is not easy to make a functioning flower clock, people have done it. There is one in his hometown of Uppsala, for instance. It has been made in the classroom (pdf) and one can pretty easily find locally useful lists of plants to try to build one.

Linnaeus; in writings titled Philosophia Botanica wrote about 3 types of flowers:1. Meteorici, A category which changes their opening and closing times according to the weather conditions.
2. Tropici, Flowers which change their opening and closing specifically to the length of the day.
3. Aequinoctales, Most important here to this story, are the flowers having fixed times for opening and closing, regardless of weather or season.

It is only those last ones that could be used for buildiing Floral Clocks, while the first two groups were important for the studies of vernalization and photoperiodism in plants in the early 20th century.

You can find some more detail of the flower clock history here. And the idea of a flower clock was also picked up by artists of various kinds:

Linnaeus’s idea for a collection of flowers that opened or closed at a particular time of day was taken up by the French composer Jean Fran aix in his composition L’horloge de flore (The Flower Clock), a concerto for solo oboe and orchestra.———————

A floral clock features in the fictional city of Quirm, in Soul Music, one of the books in Terry Pratchett’s Discworld series.

Clock Classics: It All Started with the Plants

I originally published this post on May 29, 2008.

In the old days, when people communed with nature more closely, the fact that plants and animals did different things at different times of day or year did not raise any eyebrows. That’s just how the world works – you sleep at night and work during the day, and so do (or in reverse) many other organisms. Nothing exciting there, is it? Nobody that we know of ever wondered how and why this happens – it just does. Thus, for many centuries, all we got are short snippets of observations without any thoughts about causes:

“Aristotle [noted] that the ovaries of sea-urchins acquire greater size than usual at the time of the full moon.”(Cloudsley-Thompson 1980,p.5.)

“Androsthenes reported that the tamarind tree…, opened its leaves during the day and closed them at night.”(Moore-Ede et al. 1982,p.5.)

“Cicero mentioned that the flesh of oysters waxed and waned with the Moon, an observation confirmed later by Pliny.”(Campbell 1988, Coveney and Highfield 1990)

“…Hippocrates had advised his associates that regularity was a sign of health, and that irregular body functions or habits promoted an unsalutory condition. He counseled them to pay close attention to fluctuations in their symptoms, to look at both good and bad days in their patients and healthy people.”(Luce 1971,p.8.)

“Herophilus of Alexandria is said to have measured biological periodicity by timing the human pulse with the aid of a water clock.”(Cloudsley-Thompson 1980, p.5.)

“Early Greek therapies involved cycles of treatment, known as metasyncrasis….Caelius Aurelianus on Chronic and Acute Diseases…describes these treatments.. .”(Luce 1971, p.8.)

“Nobody seems to have noticed any biological rhythmicities throughout the Middle Ages. The lone exception was Albertus Magnus who wrote about the sleep movements of plants in the thirteenth century” (Bennet 1974).

The first person to ask the question – and perform the very first experiment in the field of Chronobiology – was Jean-Jacques d’Ortous de Mairan, a French astronomer. What did he do?

In 1729, intrigued by the daily opening and closing of the leaves of a heliotrope plant (the phenomenon of ‘sleep in plants’ was well known due to Linneaus), de Mairan decided to test whether this biological “behavior” was simply a response to the sun. He took a plant (most likely Mimosa pudica but we do not know for sure as Linnean taxonomy came about a decade later) and placed it in a dark closet. He then observed it and noted that, without having access to the information about sunlight, the plant still raised its leaves during the day and let them droop down during the night.

However, De Mairan was an astronomer busy with other questions:

“….about the aurora borealis, and the relation of a prism’s rainbow colors to the musical scale, and the diurnal rotation of the earth, and the satellites of Venus, and the total eclipse of the sun that had occurred in 1706. He would waste no time writing to the Academy about the sleep of a plant!”(Ward 1971,p.43.)

He did not wanted to waste his time writing and publishing a paper on a mere plant. So his experiment was reported by his friend Marchant. It was not unusual at that time for one person to report someone else’s findings. Marchand published it in the Proceedings of the Royal Academy of Paris as he was a member, and the official citation is: De Mairan, J.J.O. 1729. Observation Botanique, Histoire de l’Academie Royale des Sciences, Paris, p.35.

In the paper Marchant wrote:

“It is well known that the most sensitive of the heliotropes turns its leaves and branches in the direction of the greatest light intensity. This property is common to many other plants, but the heliothrope is peculiar in that it is sensitive to the sun (or time of day) in another way: the leaves and stems fold up when the sun goes down, in just the same way as when touches or agutates the plant.

But M. de Mairan observed that this phenomenon was not restricted to the sunset or to the open air; it is only a little less marked when one maintains the plant continually enclosed in a dark place – it opens very appreciably during the day, and at evening folds up again for the night. This experiment was carried out towards the end of one summer, and well duplicated. The sensitive plant sense the sun without being exposed to it in any way, and is reminiscent of that delicate perception by which invalids in their beds can tell the difference between day and night. (Ward 1971)”

Marchant and de Mairan were quite careful about not automatically assuming that the capacity for time measurement resides within the plant. They could not exclude other potential factors: temperature cycles, or light leaks, or changes in other meteorological parameters.

Also, the paper, being just a page long (a “short communication”, see image to the right), does not provide detailed “materials and methods” so we do not know if “well repeated” experiments meant that this was done a few times for a day or two, or if the same plants were monitored over many days. We also do not know how, as well as how often and when, did de Mairan check on the plants. He certainly missed that the plants opened up their leaves a little earlier each day – a freerunning rhythm with a period slightly shorter than 24 hours – a dead giveaway that the rhythm is endogenous.

The idea that clocks are endogenous, residing inside organisms, was controversial for a very long time – top botanists of Europe were debating this throughout the 19th century, and the debate lasted well into the 1970s with Frank Brown and a few others desperately inventing more and more complicated mathematical models that could potentially explain how each individual, with its own period, could actually be responding to a celestial cue (blame Skinner and behaviorism for treating all behaviors as reactive, i.e., automatic responses to the cues from the environment).

The early 18th century science did not progress at a speed we are used to today. But the paper was not obscure and forgotten either – it just took some time for others to revisit it. And revisit it they did. In 1758 and 1759 two botanists repeated the experiment: both Zinn and Duhamel de Monceau (Duhamel de Monceau 1758) controlled for both light and temperature and the plants still exhibited the rhythms. They used Mimosa pudica, which suggests to us today that this was the plant originally tested by de Mairan.

Suspecting light-leaks in de Mairan’s experiment, Henri-Louis Duhamel du Monceau repeated the same experiment several times (Duhamel du Monceau 1758). At first, he placed the plants inside an old wine cave. It had no air vent through which the light could leak in, and it had a front vault which could serve as a light lock. He observed the regular opening and closing of the leaves for many days (using a candle for observation). He once took a plant out in the late afternoon – which phase-shifted the clock with a light pulse. The plant remained open all night (i.e.., not directly responding to darkness), but then re-entrained to the normal cycle the next day. Still not happy, he placed a plant in a leather trunk, wrapped it in a blanket and placed it in a closet inside the cave – with the same result: the plant leaves opened and closed every day.

So, he was convinced that no light leaks were responsible for the plant behavior. Yet he was still not sure if the temperature in the cave was absolutely constant, so he repeated the experiment in a hothouse where the temperature was constant and quite high, suspecting that perhaps a night chill prompted the leaves to close. He had to conclude: “I have seen this plant close up every evening in the hothouse even though the heat of the stoves had been much increased. One can conclude from these experiments that the movements of the sensitive plant are dependent neither on the light nor on the heat” (Duhamel de Monceau 1758). He did not know it at the time, of course, but he was the first to demonstrate that circadian rhythms are temperature compesated – the period is the same at a broad range of constant temperatures.

The research picked up speed in the 19th century. Augustus Pyramus de Candolle repeated the experiments while making sure not just that the darkness was absolute and the temperature constant, but also that the humidity was constant, thus eliminating another potential cue. He then showed that the period of diurnal movements of Mimosa is very close to 24 hours in constant darkness, but around 22 hours in constant light (using a bank of six lamps). He also managed to reverse day and night by using artificial light to which the plants responded by reversing their rhythms (De Candolle 1832) after the initial few days of “confusion”.

Another astronomer, Svante Arrhenius argued that a mysterious cosmic Factor X triggered the movements (Arrhenius 1898). He attributed the rhythms to the “physiological influence of atmospheric electricity”. Charles Darwin published an entire book on the Movement of Plants in 1880, arguing that the plant itself generates the daily rhythms (Darwin 1880).

The most famous botanist of the 19th century, Wilhelm Pfeffer, started out favouring the “external hypothesis”, arguing that light leaks were the source of external information for de Mairan’s and Duhamel’s plants (Pfeffer 1880, 1897, 1899). But his own well-designed experiments (as well as those of Darwin) forced him to change his mind later in his career and accept the “internal” source of such rhythmic movements. Unfortunately, Pfeffer published his latter views in an obscure (surprisingly, considering the short and catchy title) German journal Abhandlungen der Mathematisch-Physischen Klasse der Königlich Sächsischen Gesellschaft der Wissenschaften, so most people were (and still are) not aware that he changed his mind on this matter.

In the early 20th century, Erwin Bunning was the first to really thoroughly study circadian rhythms in plants and to link the daily rhythms to seasonality. He and many others at the time mostly studied photoperiodism and vernalization in plants, two phenomena then thought to be closely related (we know better today). For the rest of the century, animal research took over and only recently, with the advent of molecular techniques in Arabidopsis, has the plant chronobiology rejoined the rest of the field.

Here is a movie of Mimosa pudica closing its leaves due to mechanical stimulation:

And here you can see a movie of a plant sleeping and waking over several cycles (you can download an even better one here).

References:

Arrhenius, S. 1898. Die Einwirkung kosmicher Einflusse auf physiologische Verhaltnisse. Skandinavisches Archiv fur Physiologie, Vol. VIII.
Bennett, M.F. 1974. Living Clocks in the Animal World. Charles C Thomas – Publisher.
Campbell, J. 1988. Winston Churchill’s Afternoon Nap: a Wide Awake Inquiry into the Human Nature of Time. Aurum, London.
Cloudsley-Thompson, J. 1980. Biological Clocks, Their Functions in Nature. Weidenfeld & Nicolson, London.
Coveney, P. and R.Highfield, 1990. The Arrow of Time: A Voyage Through Science to Solve Time’s Greatest Mystery. Fawcett Columbine, New York.
Darwin, C. 1880. The power of movement in plants (assisted by F. Darwin). Murray, London.
De Candolle, A.P. 1832. Physiologie Vegetale. Paris: Bechet jeune.
Duhamel de Monceau, H.L. 1758. La Physique des Arbres. Paris: H.L.Guerin & L.F.Delatour.
Luce, G.G. 1971. Biological Rhythms in Human & Animal Physiology. Dover, NY.
Moore-Ede, M.C., F.M.Sulzman and C.A.Fuller. 1982. The Clocks That Time Us. Harvard University Press.
Pfeffer, W.F.P. 1880, 1897, 1899, (reprinted1903.,1905.), Pfeffer’s Physiology of Plants, Volumes I -III, Ed. and Trans. Alfred J.Ewert., Oxford .
Ward, R.R. 1971. The Living Clocks. Alfred A. Knopf, New York.


Chestnut Tree Circadian Clock Stops In Winter

I originally published this on June 26th, 2006.

The persistence of circadian rhythmicity during long bouts of hibernation in mammals has been a somewhat controversial topic in the literature. While some studies suggest that circadian clock is active during hibernation, other studies dispute this. Apparently, the truth is somewhere in-between – it differs between species:

Not all hibernating animals retain apparent circadian rhythmicity during the hibernation season. Whereas some species, such as bats and golden-mantled ground squirrels, maintain circadian rhythmicity in Tb [core body temperature] throughout the hibernation season when held in constant conditions, other species, such as European hamsters, Syrian hamsters, and hedgehogs, lose circadian rhythmicity in Tb.

The outputs of the clock measured in these studies range from body temperature and brain temperature, to timing of waking, to metabolic and behavioral parameters. But, to my knowledge, nobody has yet looked if the circadian pattern of expression of “core clock gene” persists during hibernation.

Thus, it was really interesting to see a study on the state of hibernation in a completely different kind of organism – a tree. About a year ago [Note: that was in 2005, this is a re-post from the archives], a group from Spain did exactly what was needed – they measured the levels of expression of circadian clock genes in the chestnut tree.

They measured the expression of clock genes both during naturally occurring winter dormancy and in the laboratory experiments involving chilling of seedlings combining with exposure to different photoperiods. In both cases, the core molecular mechanism of the circadian clock stopped entirely if the temperature and photoperiod both indicated ‘winter’, and was revived by warming-up the seedlings or the onset of spring.

Circadian clocks exhibit temperature independence, i.e., the period of the rhythm is not affected by temperature, within relatively broad limits. Apparently, the winter temperatures are outside the lower limit in the chestnut tree. Furthermore, it appears that the chestnut actively stops the clock with the onset of winter.

How can we interpret these data?

Overwintering is the stage in which all energetically expensive processes are minimized or shut down. However, workings of the clock itself are not very energetically expensive, so this is an unlikely reason for the elimination of rhythmicity during winter.

Second interpretation would be that, as the tree shuts down all its processes, there is nothing for the clock to regulate any more. There is also no feedback from the rest of metabolism into the clock. Thus, circadian rhythmicity fades as a by-product of overall dormancy of the plant.

Third, the clock itself may be a part of the mechanism that keeps everything else down. In other words, a clock stopped at (for instance – this is a random choice of phase) midnight will keep giving the midnight signal to the rest of the plant for months on end, keeping all the other processes at their normal midnight level (which may be very low). Thus, the clock may be central to the overall mechanism of hibernation in trees – i.e., the autumnal stopping of the clock is an evolved adaptation.

Berry Go Round – send in your posts for the next botanical blog carnival

Berry Go Round is a blog carnival devoted to highlighting recent blog posts about any aspect of plant life.

If you have published a blog post about plants since the last issue on January 30th, send me the link by using this submission form.

Officially, the deadline for submissions is February 25th, but I am lenient – even if you send it as late as 28th at noon, I will still likely include it, and will post the carnival on the morning of the 29th of February. But sending early is appreciated. If you see a post by someone else that you think fits the concept, send it in (but insert a note to me that it is not your own post).

What counts? The official ‘rules’ state:

Berry Go Round covers all thing botanical. That is, featured articles should just be about plants, from cells & chemistry to plant ecology and communities. Pictures can also be submitted whenever a minimum amount of information is given (such as scientific name, family and the like), and recipes may also be featured if the main ingredient is a plant and provided a decent botanical account follows.

So yes – small plants, big plants, common plants, rare plants, extinct or extant, mosses, liverworts, horsetails, ferns, with or without flowers, microscopic or giant trees – all of them are eligible. Biochemistry, molecular, cellular and developmental biology, physiology, behavior (yup, plants behave), evolution, genetics, paleontology, biogeography, taxonomy/systematics, ecology, conservation – anything goes. It can focus on a recent finding, or a historical account, it can explain the basics, or it can be a timeless truth, it can be basic or applied, or you can write a personal account of awe in encountering a baobab for the first time in your life.

Apart from text, we welcome original art, illustration, photography, cartoons, podcasts, videos, animations, infographics or any other forms of multimedia (especially if all mixed into a single post). If you are using someone else’s art, please properly credit and link to the original artist in your posts.

The wonderful quail…and what Sen.Coburn should learn about it.

Senator Tom Coburn (R-OK) released his “Wastebook” a week ago – a list of 100 government-funded projects that are supposedly a waste of money.

Every campaign season, quite predictably, someone from the GOP makes a document like this, listing examples of spending that, in their view, represents the most egregious excesses of governmental spending. Counting on their voters not to know or understand anything about these projects (especially the way these are carefully framed) and aware that nobody in the mainstream media will be pointing and laughing at them, they push these memes onto the unsuspecting public.

Many of these projects are competitive grant-funded scientific research, already paid by NIH or NSF after a draconian process of peer-review of the grant proposals by the experts in the field.

Remember the autism fruitfly research that Sarah Palin thought was wasteful? John McCain’s deriding of important bear DNA research? The “projector” at the Adler Planetarium? All horrendous misinterpretations of the actual research for the sake of scoring political points.

Just a campaign tactic to get people riled up against the “pointy-heads”.

Unsurprisingly, this latest list contains quite a few volleys against science – in service of politicking. A quick scan finds about a dozen scientific research projects already funded by federal grants, and I think some of the other bloggers on the network may cover some of them. I will focus on this one:

23) Rockin’ Robins: Study Looks for Connections Between Cocaine and Risky Sex Habits of Quail – (KY) $175,587

What common sense suggests, science has confirmed over and over again: namely, that cocaine use is linked to increased risky sexual behavior. Just to be sure, however, one federal agency thought it should test the hypothesis on a new subject: Japanese quail.

The University of Kentucky received a grant of $181,406 in 2010 from the National Institute of Health to study how cocaine enhances the sex drive of Japanese quail. In 2011, grant funding was extended and an additional $175,587 was provided for the study. The total awarded to the project will be $356,933.140

The study seeks to verify the clinical observations that indicated that cocaine use in humans may increase sexual motivation, thereby increasing the likelihood of the occurrence of high-risk sexual behavior. The researcher conducting the study highlighted how Japanese quail are ‘ideal‘ animals to use when studying the link between sex and drugs because the birds readily engage in reproductive behavior in the laboratory. University of Kentucky‘s website stated that quail provide a convenient and interesting alternative to standard laboratory rats and pigeons. This study is slated to continue through 2015.

Scicurious goes in great depth and detail about this particular line of research and why it is important – check it out. I will instead point out what’s wrong about laughing at Japanese quail as a research model, since I spent ten years of my life doing research on it.

Let me start with the first statement that this research is done “on a new subject: Japanese quail”. Maybe it is new to Coburn, but Japanese quail has been a pretty standard laboratory animal for about a century. Not wanting to dig through my file cabinets to find several dozen additional reviews on printed paper, I just did a quick Google Scholar search and found these few reviews on the usefulness and importance of this species in research: J.R.Cain and W.O.Cawley, 1914, Padgett, CA and Ivey, WD, 1959, Ellen P. Reese and T. W. Reese, 1962, A. E. Woodard, H. Abplanalp, W. O. Wilson, and P. Vohra, 1973, Ichilcik R and Austin JC., 1978, Huss D, Poynter G and Lansford R., 2008, Greg Poynter, David Huss and Rusty Lansford, 2009, Gregory F. Ball and Jacques Balthazart, 2010.

Note that these reviews span about a century. That’s not “new”.

Also note that most of these reviews are behind the paywalls.

Not everyone in the country is deeply ideological. Most of the US voters are intelligent and open-minded. Every couple of years they need to go to the polls so they want to be making informed decisions. They will look for information, but will not spend too much time and effort (and certainly not money) finding it. So, it is deplorable that the side of reason, the Reality-Based community, is keeping its information hidden behind paywalls, while the side of Anti-Science is not just making it all free, but actively pushing their disinformation by every avenue and channel available. Why is it a surprise that the guys who deny reality keep winning? It is easy for snake-oil salesmen to make fun of stuff that most people cannot even access to read!

Why is Japanese quail such a good laboratory animal?

Japanese quail is sometimes called the “mouse of bird research”. The two species are comparable in a number of important properties (see: Breeding Strategies for Maintaining Colonies of Laboratory Mice – A Jackson Laboratory Resource Manual; Japanese Quail As A Laboratory Animal – Avian Genetic Resource Laboratory (AGRL); Quail – AnimalResearch.info).

For example, gestation in mice lasts 18-21 days. In quail, the eggs hatch in 16-17 days. Those are both extremely fast developmental times, making it easy to quickly breed a lot of experimental animals.

It takes about six weeks for both mice and quail to attain sexual maturity after they are born. Again, that is a very fast maturation rate, making it efficient for breeding in the lab.

Mice can have litters anywhere between two and 12 pups at a time. Quail can lay essentially an egg per day throughout the year, throughout their lives. Quail win on this one – they can produce much more offspring per year. Efficient.

While techniques for genetic manipulation in quail lagged behind those of mice (just like those of mice lagged by many years behind Drosophila techniques), they are now available. It is now possible to make transgenic quail and use them in genetic research.

In many other aspects, quail is a better lab animal than the mouse (or rat or chicken). While laboratory strains of mice have been “domesticated” for only a few decades, the quail has been fully domesticated for about 500 years – it is poultry. While lab mice will rarely bite, they have to be handled with care – on the other hand, you can CUDDLE with a quail if you want to!

A decade ago, cuddling with quail.

Unlike its wild counterparts which are long-distance migrants, laboratory strains of Japanese quail are very slow fliers. Unlike wild songbirds (that need to be caught outside which is stressful) which, if they get lose in the lab one needs an army of technicians with butterfly nets to catch it (stressed), I can’t even remember how many times I caught runaway quail in mid-flight, with one hand, barely looking (actually, many times I caught them in the dark, not seeing but just hearing and feeling where they might be flying). Then you huddle it, and pet it on the head and put it back in its cage. And you get a loving look back and perhaps a quail-style “thank you” call. They are cute. But not as cute as many other species of birds, which makes it somewhat easier to overcome one’s reluctance to occasionally do something unpleasant to them, e.g., surgeries.

It is a hardy animal, very easy to keep, breed and feed, with minimal demands (which is why so many small farmers breed them around the world). They are social animals so they can be kept in groups. They are small and generally happy and content, so many more quail can be kept in a room without being stressed than, for example, one can keep comparatively enormous, slow-breeding, slow-maturing chicken in the room of the same size.

The lab rodents, like mice, have to be handled with utmost care, always keeping the threat of zoonozes in mind – there are many diseases that can jump from mice to human and back. There is essentially nothing that can infect both a human and a quail, especially not in the isolated, climate-controled environments of a university laboratory.

Quail’s immune system is amazing. While one has to perform a completely sterile surgery on mice, in quail it is done so only because IACUCs (Institutional Animal Care and Use Commitees) recently started demanding this (discussion of the wastefulness of this approach can be left for some other time). I bet you could do a surgery on a quail with dirty fingers and a rusty pocket-knife and the only consequence would be that the bird’s white blood cells would heartily laugh at you. This is also the reason why quail has been under intense research in Immunology for decades – if we learn something how the quail can be so resistant to essentially anything and everything in its environment, perhaps we can apply some of that knowledge to human medicine as well.

On the “intelligence scale” of birds, the quail hits the rock bottom. It is, frankly, not that smart. And this is a good thing from the point of view of research on behavioral neuroscience. They “don’t do” much thinking. They essentially go through the day like little automatons and most of their behaviors are routinized and stylized and automatic, like ‘fixed-action patterns’. Thus, manipulating a particular brain area usually results in a particular change of a particular behavior. This is repeatable and replicable, without too much noise in the data (at least in comparison to some other species), so the statistics are reasonably easy to do and findings are pretty clear. This makes research useful and efficient – sample sizes can be reasonably small.

There are very few species of animals about which we know as much as we do, and in so many areas of biology, as we understand the quail: embryonic development, genetics, physiology, metabolism, reproduction, immunology, endocrinology, neurobiology and behavior. With such a large amount of background information, it is much easier to make breakthroughs than when one is just starting to explore a new animal model (though as my regular readers know – I am very much in favor of adopting new models, as well as just purely comparative research). Studying effects of cocaine on reproductive behavior is so much more efficient in a species in which we do not have to start from scratch – we already know so much about its brain, behavior and reproduction, we can move on to more sophisticated studies than just the first exploratory “basic experiments”. Thus we can make faster progress. This is an efficient approach.

Most research on quail has – and often the same experiment simultaneously – relevance to three different areas of human interest: understanding of basic biology, application to human biomedical research, and application for agriculture – remember that quail is poultry.

Quail and chicken are very closely related. Each one of their genes is about 99% identical. In many ways, the quail is a model for the chicken. Instead of keeping just a few large, slow-breeding chickens in the lab, doing one slow experiment at the time, one can instead keep hundreds of quail in the same amount of space without stress, and do several fast, simultaneous experiments in the same amount of time. That is efficient. And that is how we can learn how to increase chicken (and turkey) productivity AND at the same time study how to make them healthy, unstressed and happy while doing so – a very important aspect of Poultry Science research.

A big advantage of quail over rodents is in the research on sleep. Rodents are nocturnal. Rats and mice sleep more during the day than during the night. But their sleep is not consolidated – they sleep in many short bursts: there are just more of these bursts during the day than night. On the other hand, quail is, like us, a diurnal animal. Quail are fully awake throughout the day and have a long consolidated sleep during the night (at least in short summer nights, while they may occasionally wake up during long winter nights…wow – just like us!!!!)

Finally, my own past research combining the studies on circadian rhythms and clocks, thermoregulation, photoperiodism, seasonality and reproduction (see this for a follow-up in another species) has several areas of relevance. It helps us make smarter husbandry for the poultry industry. It is a great model for why human adolescents, once they hit puberty, have phase-delayed circadian rhythms (cannot fall asleep in the evening, then cannot wake up in the morning, just like quail). It helps to inform how to conserve endangered bird species, and to predict how the birds will respond to climate change.

Not too shabby for a small bird, right? You really want to make fun of it for the sake of politics? You are lucky the quail is just too nice to bite you back!

Related at Scientific American

Cocaine and the sexual habits of quail, or, why does NIH fund what it does?

The Guppy Project is not wasteful, Sen. Coburn.

Evolutionary Medicine: Does reindeer have a circadian stop-watch instead of a clock?

I originally posted this on April 13th, 2010.

Whenever I read a paper from Karl-Arne Stokkan’s lab, and I have read every one of them, no matter how dense the scientese language I always start imagining them running around the cold, dark Arctic, wielding enormous butterfly nets, looking for and catching reindeer (or ptarmigans, whichever animal the paper is about) to do their research.

If I was not so averse to cold, I’d think this would be the best career in science ever!

It is no surprise that their latest paper – A Circadian Clock Is Not Required in an Arctic Mammal (press release) – was widely covered by the media, both traditional and blogs. See, for example, The Scientist, BBC, Scientific American podcast and Wired Science.

Relevant, or just cool?

It is hard to find a science story that is more obviously in the “that’s cool” category, as opposed to the “that’s relevant” category. For the background on this debate, please read Ed Yong, David Dobbs, DeLene Beeland, Colin Schultz, and the series of Colin’s interviews with Carl Zimmer, Nicola Jones, David Dobbs, Jay Ingram, Ferris Jabr, Ed Yong and Ed Yong again.

I agree, it is a cool story. It is an attention-grabbing, nifty story about charismatic megafauna living in a strange wilderness. I first saw the work from the lab in a poster session at a conference many years ago, and of all the posters I saw that day, it is the reindeer one that I still remember after all these years.

Yet, the coolness of the story should not hide the fact that this research is also very relevant – both to the understanding of evolution and to human medicine. Let me try to explain what they did and why that is much more important than what a quick glance at the headlines may suggest. I did it only part-way a few years ago when I blogged about one of their earlier papers. But let me start with that earlier paper as background, for context.

Rhythms of Behavior

In their 2005 Nature paper (which was really just a tiny subset of a much longer, detailed paper they published elsewhere a couple of years later), Stokkan and colleagues used radiotelemetry to continuously monitor activity of reindeer – when they sleep and when they roam around foraging.

You should remember that up in the Arctic the summer is essentially one single day that lasts several months, while the winter is a continuous night that lasts several months. During these long periods of constant illumination, reindeer did not show rhythms in activity – they moved around and rested in bouts and bursts, at almost unpredictable times of “day”. Their circadian rhythms of behavior were gone.

But, during brief periods of spring and fall, during which there are 24-hour light-dark cycles of day and night, the reindeer (on the northern end of the mainland Norway, but not the population living even further north on Svaldbard which remained arrhythmic throughout), showed daily rhythms of activity, suggesting that this species may possess a circadian clock.

Rhythms of Physiology

In a couple of studies, including the latest one, the lab also looked into a physiological rhythm – that of melatonin synthesis and secretion by the pineal gland. Just as in activity rhythms, melatonin concentrations in the blood showed a daily (24-hour) rhythm only during the brief periods of spring and fall. Furthermore, in the latest paper, they kept three reindeer indoors for a couple of days, in light-tight stalls, and exposed them to 2.5-hour-long periods of darkness during the normal light phase of the day. Each such ‘dark pulse’ resulted in a sharp rise of blood melatonin, followed by just as abrupt elimination of melatonin as soon as the lights went back on.

Rhythms of gene expression

Finally, in this latest paper, they also looked at the expression of two of the core clock genes in fibroblasts kept in vitro (in a dish). Fibroblasts are connective tissue cells found all around the body, probably taken out of reindeer by biopsy. In other mammals, e.g., in rodents, clock genes continue to cycle with a circadian period for a very long time in a dish. Yet, the reindeer fibroblasts, after a couple of very weak oscillations that were roughly in the circadian range, decayed into complete arrhytmicity – the cells were healthy, but their clocks were not ticking any more.

What do these results suggest?

There is something fishy about the reindeer clock. It is not working the same way it does in other mammals studied to date. For example, seals and humans living in the Arctic have normal circadian rhythms of melatonin. Some other animals show daily rhythms in behavior. But in reindeer, rhythms in behavior and melatonin can be seen only if the environment is rhythmic as well. In constant light conditions, it appears that the clock is not working. But, is it? How do we know?

During the long winter night and the long summer day, the behavior of reindeer is not completely random. It is in bouts which show some regularity – these are ultradian rhythms with the period much shorter than 24 hours. If the clock is not working in reindeer, i.e., if there is no clock in this species, then the ultradian rhythms would persist during spring and fall as well. Yet we see circadian rhythms during these seasons – there is an underlying clock there which can be entrained to a 24-hour light-dark cycle.

This argues for the notion that the deer’s circadian clock, unless forced into synchrony by a 24 external cycle, undergoes something called frequency demultiplication. The idea is that the underlying cellular clock runs with a 24-hour period but that is sends signals downstream of the clock, triggering phenotypic (observable) events, several times during each cycle. The events happen always at the same phases of the cycle, and are usually happening every 12 or 8 or 6 or 4 or 3 or 2 or 1 hours – the divisors of 24 (not necessarily whole hours, e.g., 90minute bursts are also possible). Likewise, the clock can trigger the event only every other cycle, resulting in a 48-hour period of the observable behavior.

If we forget for a moment the metaphor of the clock and think instead of a Player Piano, it is like the contraption plays the note G several times per cycle, always at the same moments during each cycle, but there is no need to limit each note to appear only once per cycle.

On the other hand, both the activity and melatonin rhythms appear to be driven directly by light and dark – like a stop-watch. In circadian parlance this is called an “hourglass clock” – an environmental trigger is needed to turn it over so it can start measuring time all over again. Dawn and dusk appear to directly stop and start the behavioral activity, and onset of dark stimulates while onset of light inhibits secretion of melatonin. An “hourglass clock” is an extreme example of a circadian clock with a very low amplitude.
While we mostly pay attention to period and phase, we should not forget that amplitude is important. Yes, amplitude is important. It determines how easy it is for the environmental cue to reset the clock to a new phase – lower the amplitude of the clock, easier it is to shift. In a very low-amplitude oscillator, onset of light (or dark) can instantly reset the clock to Phase Zero and start timing all over again – an “hourglass” behavior.

The molecular study of the reindeer fibroblasts also suggests a low-amplitude clock – there are a couple of weak oscillations to be seen before the rhythm goes away completely.

There may be other explanations for the observed data, e.g., masking (direct effect of light on behavior bypassing the clock) or relative coordination (weak and transient entrainment) but let’s not get too bogged down in arcane circadiana right now. For now, let’s say that the reindeer clock exists, that it is a very low-amplitude clock which entrains readily and immediately to light-dark cycles, while it fragments or demultiplies in long periods of constant conditions.

Why is this important to the reindeer?

During long night of the winter and the long day of the summer it does not make sense for the reindeer to behave in 24-hour cycles. Their internal drive to do so, driven by the clock, should be overpowered by the need to be flexible – in such a harsh environment, behavior needs to be opportunistic – if there’s a predator in sight: move away. If there is food in sight – go get it. If you are full and there is no danger, this is a good time to take a nap. One way to accomplish this is to de-couple the behavior from the clock. The other strategy is to have a clock that is very permissive to such opportunistic behavior – a very low-amplitude clock.

But why have clock at all?

Stokkan and colleagues stress that the day-night cycles in spring help reindeer time seasonal events, most importantly breeding. The calves/fawns should be born when the weather is the nicest and the food most plentiful. The reindeer use those few weeks of spring (and fall) to measure daylength (photoperiod) and thus time their seasonality – or in other words, to reset their internal calendar: the circannual clock.

But, what does it all mean?

All of the above deals only with one of the two hypotheses for the adaptive function (and thus evolution) of the circadian clock. This is the External Synchronization hypothesis. This means that it is adaptive for an organism to be synchronized (in its biochemistry, physiology and behavior) with the external environment – to sleep when it is safe to do so, to eat at times when it will be undisturbed, etc. In the case of reindeer, since there are no daily cycles in the environment for the most of the year, there is no adaptive value in keeping a 24-hour rhythm in behavior, so none is observed. But since Arctic is highly seasonal, and since the circadian clock, through daylength measurement (photoperiodism) times seasonal events, the clock is retained as an adaptive structure.

This is not so new – such things have been observed in cave animals, as well as in social insects.

What the paper does not address is the other hypothesis – the Internal Synchronization hypothesis for the existence of the circadian clock – to synchronize internal events. So a target cell does not need to keep producing (and wasting energy) to produce a hormone receptor except at the time when the endocrine gland is secreting the hormone. It is a way for the body to temporally divide potentially conflicting physiological functions so those that need to coincide do so, and those that conflict with each other are separated in time – do not occur simultaneously. In this hypothesis, the clock is the Coordination Center of all the physiological processes. Even if there is no cycle in the environment to adapt to, the clock is a necessity and will be retained no matter what for this internal function, though the period now need not be close to 24 hours any more.

What can be done next?

Unfortunately, reindeer are not fruitflies or mice or rats. They are not endangered (as far as I know), but they are not easy to keep in the laboratory in large numbers in ideal, controlled conditions, for long periods of time.

Out in the field, one is limited as to what one can do. The only output of the clock that can be monitored long-term in the field is gross locomotor activity. Yet, while easiest to do, this is probably the least reliable indicator of the workings of the clock. Behavior is too flexible and malleable, too susceptible to “masking” by direct effects of the environment (e.g., weather, predators, etc,). And measurement of just gross locomotor activity does not tell us which specific behaviors the animals are engaged in.

It would be so nice if a bunch of reindeer could be brought into a lab and placed under controlled lighting conditions for a year at a time. One could, first, monitor several different specific behaviors. For example, if feeding, drinking and defecation are rhythmic, that would suggest that the entire digestive system is under circadian control: the stomach, liver, pancreas, intestine and all of their enzymes. Likewise with drinking and urination – they can be indirect indicators of the rhythmicity of the kidneys and the rest of the excretory system.

In a lab, one could also continuously monitor some physiological parameters with simple, non-invasive techniques. One could, for example monitor body temperature, blood pressure and heart-rate, much more reliable markers of circadian output. One could also take more frequent blood samples (these are large animals, they can take it) and measure a whole plethora of hormones along with melatonin, e.g., cortisol, thyroid hormones, progesterone, estrogen, testosterone, etc (also useful for measuring seasonal responses). One could measure metabolites in urine and feces and also gain some insight into rhythms of the internal biochemistry and physiology. All of that with no surgery and no discomfort to the animals.

Then one can place reindeer in constant darkness and see if all these rhythms persist or decay over time. Then one can make a PhaseResponse Curve and thus test the amplitude of the underlying oscillator (or do that with entrainment to T-cycles, if you have been clicking on links all along, you’ll know what I’m talking about). One can test their reproductive response to photoperiod this way as well.

Finally, fibroblasts are peripheral cells. One cannot expect the group to dissect suprachiasmatic nuclei out of reindeer to check the state of the master pacemaker itself. And in a case of such a damped circadian system, testing a peripheral clock may not be very informative. Better fibroblasts than nothing, but there are big caveats about using them.

Remember that the circadian system is distributed all around the body, with each cell containing a molecular clock, but only the pacemaker cells in the suprachiasmatic nucleus are acting as a network. In a circadian system like the one in reindeer, where the system is low-amplitude to begin with, it is almost expected that peripheral clocks taken out of the body and isolated in a dish will not be able to sustain rhythms for very long. Yet those same cells, while inside of the body, may be perfectly rhythmic as a part of the ensemble of all the body cells, each sending entraining signals to the others every day, thus the entire system as a whole working quite well as a body-wide circadian clock. This can be monitored in real-time in transgenic mice, but the technology to do that in reindeer is still some years away.

Finally, one could test a hypothesis that the reindeer clock undergoes seasonal changes in its organization at the molecular level by comparing the performance of fibroblasts (and perhaps some other peripheral cells) taken out of animals at different times of year.

What’s up with this being medically relevant?

But why is all this important? Why is work on mice not sufficient and one needs to pay attention to a strange laboratory animal model like reindeer?

First, unlike rodents, reindeer is a large, mostly diurnal animal. Just like us.

Second, reindeer normally live in conditions that make people sick, yet they remain just fine, thank you. How do they do that?

Even humans who don’t live above the Arctic Circle (or in the Antarctica), tend to live in a 24-hour society with both light and social cues messing up with our internal rhythms.

We have complex circadian systems that are easy to get out of whack. We work night-shifts and rotating shifts and fly around the globe getting jet-lagged. Jet-lag is not desynchronization between the clock and the environment, it is internal desynchronization between all the cellular clocks in our bodies.

In the state of almost permanent jet-lag that many of us live in, a lot of things go wrong. We get sleeping disorders, eating disorders, obesity, compromised immunity leading to cancer, problems with reproduction, increase in psychiatric problems, the Seasonal Affective Disorder, prevalence of stomach ulcers and breast cancer in night-shift nurses, etc.

Why do we get all that and reindeer don’t? What is the trick they evolved to stay healthy in conditions that drive us insane and sick? Can we learn their trick, adopt it for our own medical practice, and use it? Those are kinds of things that a mouse and a rat cannot provide answers to, but reindeer can. I can’t think of another animal species that can do that for us. Which is why I am glad that Stokkan and friends are chasing reindeer with enormous butterfly nets across Arctic wasteland in the darkness of winter 😉

Reference:

Lu, W., Meng, Q., Tyler, N., Stokkan, K., & Loudon, A. (2010). A Circadian Clock Is Not Required in an Arctic Mammal Current Biology, 20 (6), 533-537 DOI: 10.1016/j.cub.2010.01.042

Images: Reindeer drawing – EnchantedLearning.com; Reindeer photos – Reindeer Ranching and the Economic Benefits, by Emma Englesby, Kimberly Richards and Stephanie Bell; graphs from the Lu et al. 2010.

Related at Scientific American:

Rudolph Would Have Run Away From Santa by Jason G. Goldman

A Skill Better Than Rudolph’s by Anne-Marie Hodge

How Its Internal Clock Is Read, Knows Reindeer by Christopher Itagliata (podcast)

How Rudolph Remains Bright-Eyed and Bushy-Tailed Through the Big Night by David Biello

Trying to keep Rudolph, and his fellow reindeer, from going down in history by John R. Platt

Satellite snow maps help reindeer herders adapt to a changing Arctic, From ESA.

U.S. Seeks to Protect Forests to Save Wild Reindeer by Laura Zuckerman

The New Meanings of How and Why in Biology?

If you ask a biologist for an explanation for a trait of an organism, you will get different answers depending on what kind of biologist you asked.

One biologist will give you an explanation in terms of molecules, cells, tissues, organs, organ systems and the organism as a whole, explaining how that trait develops in the embryo and how it works in the adult.

The other biologist may give you an explanation of how that trait arose within that particular lineage, why it was selected, how it confers fitness to the organism, and why that trait is considered to be an adaptation.

For about a century following Darwin’s ‘Origin of Species’, confusion reigned in biology as to which kind of explanation is the “real” explanation. Biologists misunderstood each other, talked past each other, and entered sometimes fierce debates when trying to explain biological phenomena.

As early as 1937, James Baker (who was an early researcher in my field, although he did not know it at the time, studying bird seasonality, latitude, reproduction and migration) suggested that biology asks two kinds of questions which are different, yet compatible with each other. The ‘How’ questions explain the mechanism by which a trait develops and works (physiological explanation) and the ‘Why’ questions explain the evolutionary history and adaptive function of the trait.

In 1961, Ernst Mayr published a very influential paper – ‘Cause and effect in biology’ – in Science in which (also using bird migration as an example) he named the ‘How’ questions ‘Proximate causes’ (how the birds’ brains orient and navigate) and the ‘Why’ questions ‘Ultimate causes’ (how did the birds evolve to start their long-distance migrations). In the paper Mayr argued that these two kinds of questions are separate domains of study, yet that they are compatible and that each informs the other. Evolutionary theorists and philosophers of science ran with this idea, and it quickly became almost universally accepted, entered the textbooks and has been taught in introductory biology courses ever since.

Two years later (1963), Niko Tinbergen published a paper that was a refinement of this idea, which became even more influential than Mayr’s among people studying animal behavior. In the paper, Tinbergen proposed that every biological phenomenon should be studied by asking four questions: mechanism (physiology), development, function, and evolutionary history. The former two are subsets of Proximate causes, and the latter two are subsets of Ultimate causes. Tinbergen argued that the only way to properly understand a trait is if one asks ALL four questions and let the answers to one question inform the research on the other three and so on, in an iterative manner, until the phenomenon is fully understood.

In today’s issue of Science, there is an interesting new paper by philosophers of biology Kevin Laland, Kim Sterelny, John Odling-Smee, William Hoppitt and Tobias Uller. In it, the authors argue that the sharp dichotomy between Proximate and Ultimate questions as stated by Mayr and accepted by many (but not all) biologists may not be as useful any more (while acknowledging it was useful at the time, if nothing else to settle the old disputes stemming from mutual misunderstandings as to what constitutes ‘explanation’ in biology).

In science, as in many other areas, words matter. Words are metaphors that put us in a particular frame of mind. Different frames of mind guide different approaches to research questions. Thus, re-evaluating scientific metaphors as used by researchers is an important exercise that all fields should do every now and then (like I did for my field yesterday).

The distinction between Proximate and Ultimate questions, especially in the strong version as envisioned by Mayr, suggests a uni-directional causation of biological traits – genes code for traits. Once developed in the individuals, the traits become visible to natural selection and can be selected for or against. The causation always flows from Proximate to Ultimate domain.

But, as the new paper reminds us, last several decades of research have shown that there are many aspects of biology in which this clean separation – and especially the single direction – does not work. The authors use examples of evo-devo, sexual selection, niche construction, evolution of human cooperation, and cultural evolution, in which development and physiology affect the evolution and vice versa.

In sexual selection, male and female traits (e.g., males’ long tails in peacocks and females’ preferences for long tails in peahens) affect each others selection, thus directs evolution in a small particular subset of all possible directions.

In niche construction, parents modify the environment in a way that affects the fitness of their progeny. They use the example of earthworms which change the physical and chemical properties of the soil. After such changes were effected by their parents, the offspring find themselves in a different selective environment than their parents. Given many generations, mechanistic trait (what earthworms do to the soil) changes the direction in which evolution proceeds. In many cases, the activities of one species affect the environment, and thus selective pressures, for other species in the same space.

While some researchers think of cultural evolution as a higher-level evolutionary process, others see it as a proximate cause that affects biological evolution. Just like in niche construction, transmission of cultural traits (e.g., knowledge and skills) affects the way humans live and work, thus altering the environment (living in big cities makes it less likely to get eaten by a lion, but more likely to get hit by a car, or die young due to stress) which now selects for different sets of traits.

The paper does not argue we should abandon the terms Proximate and Ultimate. The authors acknowledge that there will always be How and Why questions in biology, and that the two sets of questions are complementary and inform each other. What they argue is that straightforward causation from genes through development to traits visible to selection is rare in nature, more of an exception than the rule.

They suggest that, instead, we should change the way we think when we use the words “Proximate” and “Ultimate”. Proximate (How) questions are not limited to genes, development and physiology. And Ultimate (Why) questions are not limited to adaptive function and evolutionary history. The answers to both the How and the Why questions will almost always have both mechanistic and evolutionary components.

What they do not say explicitly is that this suggestion to change the way we think about How and Why questions is going to affect the way we do research and understand nature. In a paradigm in which developmental and evolutionary causes undergo multiple feedback loops of mutual effect, the notion of “gene control” (or as philosophers would say “upward causation”, or bad journalists would say “gene for X”) would be replaced by a more sophisticated and more realistic understanding of the world in which explanations reside simultaneously at multiple levels, and “control” can be both upward and downward.

In an effort to attract not only creationists but also climate change denialists and anti-vaccers in the comments, I should also note one more thing that is missing from the paper – why should we care about all of this?

And there is something very obvious going on in the world right now. Cultural evolution in humans has led to accumulation across generations of knowledge and skills that have profoundly affected the way we live. From the advances in medicine (especially germ theory leading to better public health, hygiene, vaccines and antibiotics) leading to a huge increase in survivability and longevity of humans leading to population explosion, to the way we find, transform and use energy, our newly developed behaviors have all resulted in large effects humans exert on the environment of other species.

While clear-cutting a forest affects local populations, global warming affects them all. We are in a midst of the grandest experiment of niche construction to ever happen on this planet. So perhaps we should think about it in a correct and realistic way – not just as cultural evolution we can be proud of, but also as a proximate cause of trials and tribulations of all the other organisms on Earth.

One final note – much of the stuff in this paper is not that new (though concisely and clearly stated here, for a change). It is not new to people who have been carefully reading journal papers and books in philosophy of biology over the past few decades. It is also not new to people who have been observing these kinds of debates between philosophers of science and theoretically minded biologists in the science blogosphere over the past several years. But by being published in Science this topic is now brought to the new audiences that are not familiar with either philosophical literature or the blogosphere – the thousands of researchers who are still limiting their information intake to journals like that. And it is useful for that audience to hear these ideas, too.

Reference:

Kevin N. Laland, Kim Sterelny, John Odling-Smee, William Hoppitt, Tobias Uller, Cause and Effect in Biology Revisited: Is Mayr’s Proximate-Ultimate Dichotomy Still Useful? Science, Vol. 334, December 6, 2011.

The Clock Metaphor

Originally published on June 30, 2009.

Chad Orzel wrote a neat history of (or should we say ‘evolution of’) clocks, as in “timekeeping instruments”. He points out the biological clocks are “…sort of messy application, from the standpoint of physics…” and he is right – for us biologists, messier the better. We wallow in mess, cherish ambiguity and relish complexity. Anyway, he is talking about real clocks – things made by people to keep time. And he starts with a simple definition of what a clock is:

In order to really discuss the physics of timekeeping, you need to strip the idea of a clock down to the absolute bare essentials. At its core, a clock really has only one defining characteristic: A clock is a thing that ticks.

OK, I’m using a fairly broad definition of “tick,” here, but if you’ll grant that leeway, “ticking” is the essential property of clocks. In this context, “ticking” just refers to some regular, repetitive behavior that takes place in a periodic fashion.

This reminds me that a “biological clock” is a metaphor. A useful metaphor, but a metaphor nonetheless (and just like metaphors of cellular machinery are taken literally by Creationists, they have been known on occasion to talk about circadian clocks as if they had real wheels and cogs and gears!).

I want to stress that the clock metaphor has been very useful for the study of biological rhythms. Without Pittendrigh’s insight that cycles in nature can be modeled with the math of physical oscillators, we would be probably decades behind (unless someone else of authority in the field at the time had the same insight back then) in our understanding of the underlying biology. Just check how useful it was in the entire conceptualization of entrainment and photoperiodism. The Phase-Response Curve, based on the math of physical oscillators, is the Number One tool in the chronobiological repertoire.

But, just as most people in the field take the clock metaphor for granted and without much thinking, there have been a few people who questioned its utility for some areas of research. For instance, for the study of biological rhythms in nature within an ecological and evolutionary context, Jim Enright proposed a metaphor of an audio-tape set on continuous play (Enright, J.T. (1975). The circadian tape recorder and its entrainment. In Physiological Adaptation to the Environment (ed. F.J.Vernberg), pp. 465-476. Intext Educational Publishers, Ney York.). Only a dozen or so publications since then took him seriously and tried to apply this concept. Today, in the age of CDs and iPods, who even remembers audio tapes?

While fully utilizing the utility of the clock metaphor and applying it myself in my own work, I was always cautious about it. Aware that it is a metaphor, I always wondered if it constrains the way we think about the biological process and if we may miss important insights by not thinking in terms of other possible metaphors.

While far from mature, my thinking is that different metaphors apply best to different areas of research and different questions. While the clock metaphor is great for understanding the entrainment of the circadian system (including whole organism, tissues and individual cells) and photoperiodism, and Enright’s endless tape (or some modern substitute) may be useful for ecological studies (including temporal learning and memory), other angles of study may require other concepts.

For instance, I think that the study of what goes inside the cell can benefit from a different metaphor. Studying the molecular basis of circadian rhythms may best be done by utilizing a Rube-Goldberg Machine metaphor: event A triggers event B which starts process C which results in event D….and so on until the event Z causes the event A to happen again. If that last step is missing, it is not a circadian rhythm – it is more akin to an hourglass clock in which something outside of the system needs to start the process all over again.

For studying the outputs, i.e., how the circadian system orchestrates timing of all the other processes in the body, the metaphor may have to fit the organism. An ON-OFF switch is the best metaphorical description of the clock system in (Cyano)bacteria, where there are only two states of the system: the day state and the night state.

For something a little bit more eukaryotic, a relay may be a better metaphor (more than two, but not too many states). The metaphor of a camshaft in car engines that times the opening and closing of cylinders would be fine for fungi and plants and perhaps some invertebrates.

But I had a hard time coming up with a decent metaphor that could apply to complex animals, like us. So far, the best I could come up with is the barrel of a Player Piano. Many little knobs on its surface determine when each note will be played. If you make the barrel rotate slowly and the song lasts 24 hours, then outputs from circadian pacemakers are knobs and the target organs (and peripheral oscillators in them) are those long prongs that make music. Can you think of a better metaphor?

Related reading:

Basics: Biological Clock
Circadian clock without DNA–History and the power of metaphor
A Pacemaker Is A Network
Everything You Always Wanted To Know About Sleep (But Were Too Afraid To Ask)
Seasonal Affective Disorder – The Basics
Sun Time is the Real Time
Lesson of the Day: Circadian Clocks are HARD to shift!
Lithium, Circadian Clocks and Bipolar Disorder
Are Zombies nocturnal?
Diversity of insect circadian clocks – the story of the Monarch butterfly
Me and the copperheads–or why we still don’t know if snakes secrete melatonin at night
The Mighty Ant-Lion
City Of Light: Insomniac Urban Animals
Spring Forward, Fall Back – should you watch out tomorrow morning?

Basics: Biological Clock

First published on January 28, 2007

Considering I’ve been writing textbook-like tutorials on chronobiology for quite a while now, trying always to write as simply and clearly as possible, and even wrote a Basic Concepts And Terms post, I am surprised that I never actually defined the term “biological clock” itself before, despite using it all the time.

Since the science bloggers started writing the ‘basic concepts and terms’ posts recently, I’ve been thinking about the best way to define ‘biological clock’ and it is not easy! Let me try, under the fold:

A biological clock is a structure that times regular re-occurence of biochemical, physiological and behavioral events in an organism in constant environmental conditions

Perhaps the best way to explain this is to dissect the definition word-by-word, explaining my choice of words included (and those omitted) in the definition. But first, I need to make it clear that I am NOT trying to invent a new definition, or to impose my views on others. Instead, I am trying to capture the sense in which the term has actually been used by the practitioners in the field, and the way such usage may have changed over time.

What a Biological Clock isn’t

– I need to stress once again that the term “biological clock” is not a real entity, but a metaphor used by the researchers to describe a real entity in shorthand. This metaphor was very useful throughout the history of the field, though on occasion it locks people into frames of mind that may prevent them from seeing a problem as clearly as it could be.

– A biological clock is certainly not to be taken literally, as a real machine with gears or pendulums ticking somewhere inside a living organism.

– A biological clock does not refer to the pseudoscience of biorhythms, one of many ways to extract money from the gullible, either in its original Wilhelm Fliess version or its more recent and spiced-up Oriental variety.

– Colloquially, people often use the term ‘biological clock’ in the sense of “mine is ticking” meaning that time for having kids is running out. That is fine in conversation, but it is not a scientific use of the term.

– Biological Clock should not be confused with the Molecular Clock, a measure of the rate of nucleotide substitution in the DNA over evolutionary time periods, used to infer times of divergence between lineages.

…in an organism…

There are rhythms in nature that occur at levels higher than the organism, e.g., the cycles of population booms and busts in ecology (hare and lynx examples are most famous). Such rhythms are never refered to in the scientific literature as driven by any kind of clocks. The term ‘biological clock’ is sometimes used interchangeably with the term ‘physiological clock’.

This is also the reason I left out of the definition any references to adaptive or evolutionary factors and focused on the way the term is used in the literature – as a sources of a physiological mechanism.

…in constant environmental conditions…

If I give you an electroshock every two hours, you will exhibit a 2-hour cycle of convulsions. This does not mean that your rhythm is endogenously generated by an internal biological clock. It is directly induced by a recurring event in the environment. Many rhythms in living organisms are a result of a direct effect of some environmental factor. A biological clock is responsible only for recurring events that are not direct responses to the environmental cycles.

Yet, I did not use a term “environmentally independent” or some such phrase, because the rhythms generated by endogenous clocks are malleable to environmental factors, especially to light (and very few hormones and other chemicals) – the phase, period and amplitude of the rhythms can be modified by environmental cues. They just don’t disappear once the organism is held in completely constant conditions for prolonged periods of time (at least 2-3 times longer than the period of a single cycle).

…biochemical, physiological and behavioral events…

I did not want to say “everything”, although it comes close in reality. Again, this excludes ecological cycles. It also leaves it somewhat vague if developmental events are to be included or not, which is a good thing, because some developmental events are (e.g., insect eclosion, bird hatching, somite development, developmental timing in Nematodes), while others are not regulated by various types of biological clocks.

Also, not every clock in the body controls every event. A clock in the liver times events in the liver, a clock in the lungs controls events in the lungs. Only the pacemakers control everything, by synchronizing peripheral clocks, which in turn drive local rhythms.

A pacemaker in the suprachiasmatic area (SCN) of the mammalian brain may entrain other local clocks in the brain which in turn drive rhythms of various behaviors.

…times regular re-occurence…

I did not really want to use the word “rhythm” because it may suggest only rhythms of a high frequency (as in music rhythms). I also did not want to limit the definition only to daily/circadian rhythms. Other kinds of rhythms, e.g,. tidal, lunar and circannual, are also driven by biological clocks. The term “calendar” is sometimes seen in popular articles, though not as a specific scientific term, and only in reference to photoperiodism.

…a structure…

This was the hardest part of making the definition. What is a clock? A mechanism? An organ system?

Throughout the 20th century, this was easy. You take an organism, you put it in some kind of setup in which you can continuously monitor some kind of output (usually behavioral activity) and you document a rhythm in constant conditions. Then you systematically lesion or remove various organs or nuclei in the brain, until the rhythm disappears. The organ, which when removed results in arrhytmicity is, you publish, the biological clock in that organism. Thus, you discover the SCN in mammals or the pineal or retina in non-mammalian vertebrates, various brain-nuclei, optic lobes or eyes in invertebrates, etc.

But the world has changed since then. We are now investigating biological clocks at the molecular level. Is the transcription-translation feedback loop among a dozen or so canonical clock genes itself a clock? No, because it is only a necessary but not sufficient part of the clock. Or is a cell that contains such a molecular mechanism a clock? I’d say yes. Or is the tissue composed of such cells a clock? Different people in the field use this term differently, so I wanted to remain vague. But it is a structure.
At the same time, the distinction between a clock and a pacemaker is becoming more and more important, yet more and more difficult to define.

The clock in each cell of the liver is entrained by the signals from the pacemaker in the SCN. The SCN is, in turn, entrained by the light-dark cycles detected in the environment by the eyes. Is the only distinction between a pacemaker and the peripheral clock in the ability to directly (vs.indirectly) tap into environmental information? Does that mean that we have pacemakers and clocks, while fruitflies and zebrafish have only pacemakers as every cell of their bodies is a pacemaker directly entrained by environment? Those are some of the current problems in the field. This is the reason why more and more chronobiologists tend to use the term “circadian system” instead of “circadian clock”, in order to imply the underlying complexity.

In many animals, there are not just clocks in every cell in the body, but also multiple pacemakers, each getting information from the environment. These multiple pacemakers affect each other as well as peripheral clocks and are also affected by the feedback from the periphery.

And that is just vertebrates! We know much less about clocks and circadian organization in invertebrates, fungi and plants.

And then, there are unicellular organisms, both bacteria and protists, many of which contain, or should we say, ARE biological clocks. There is no distinction there between the clock and everything else the cell does.

Recently, it has been discovered that biological clocks (or at least clock genes) are also directly involved in regulation of (not just timing of) development, metabolism, appetite, thermoregulation, reproduction, sleep, cocaine addiction and behavior. Thus, the borderlines between the circadian system and other organ systems are getting increasingly fuzzy.

So, whatever structure (cell or higher) that controls the timing of oscillations in everything happening in the body devoid of environmental cues is a biological clock.

Related reading:

Circadian clock without DNA–History and the power of metaphor
Everything You Always Wanted To Know About Sleep (But Were Too Afraid To Ask)
Seasonal Affective Disorder – The Basics
Sun Time is the Real Time
Lesson of the Day: Circadian Clocks are HARD to shift!
Lithium, Circadian Clocks and Bipolar Disorder
Are Zombies nocturnal?
Diversity of insect circadian clocks – the story of the Monarch butterfly
Me and the copperheads–or why we still don’t know if snakes secrete melatonin at night
The Mighty Ant-Lion
City Of Light: Insomniac Urban Animals
Spring Forward, Fall Back – should you watch out tomorrow morning?
A Pacemaker Is A Network

Data for #drunksci: Daily rhythm of alcohol tolerance

Everything important in our bodies cycles. Including liver enzymes. Including alcohol dehydrogenase (though DUI laws do not take this into consideration).

This data-set is from an old study (Wilson R, Newman E and Newman H. 1956. Diurnal Variation in Rate of Alcohol Metabolism. J Appl Physiol 8 556-558.), back from the times when it was OK to recruit some college freshmen to drink alcoholic beverages in the name of science (good luck in getting any IRB in the USA to let you do that today!).

This is a record of a diurnal rhythm in alcohol clearance, and the figure is from a pamphlet: Palmer JD 1983. Human Biological Rhythms. Carolina Biological Supply Company, Burlington NC.:

It shows why we can drink more in the evening than at other times of day – there is so much more alcohol dehydrogenase activity in the evening. I am not encouraging drinking here, but if you are into it and can be responsible about it, you can save some serious money by downing a single shot at dawn, according to this graph, or enjoy it more at night.

So, what do you think – does it matter at what time of day/night cops stop you to give you a breathalyzer test? Or your medical tests of various kinds?

And what do you think about the ethics of the study?

a) it was unethical to do this even back in 1956
b) it was OK according to the ethics of the day, but ethics evolves over time so it is unethical today.
c) it is ethical today, but the “ethics creep” of the IRBs has gone way over the line of common sense.

Thoughts?

Books: ‘Bonobo Handshake’ by Vanessa Woods

Originally posted on June 7, 2010.

To get disclaimers out of the way, first, Vanessa Woods (on Twitter) is a friend. I first met her online, reading her blog Bonobo Handshake where she documented her day-to-day life and work with bonobos in the Congo. We met in person shortly after her arrival to North Carolina, at a blogger meetup in Durham, after which she came to three editions of ScienceOnline conference.

I interviewed Vanessa after the 2008 event and blogged (scroll down to the second half of the post) about her 2009 session ‘Blogging adventure: how to post from strange locations’. At the 2010 conference, she was one of the five storytellers at the ScienceOnline Monti on Thursday night (and did another stint at The Monti in Carrboro a couple of months later). I have since then also met her husband Brian Hare and we instantly hit it off marvelously.

I have read Vanessa’s previous book, ‘It’s every monkey for themselves‘, but never reviewed it on the blog because I felt uneasy – that book is so personal! But it is an excellent and wonderfully written page-turner of a book so I knew I was in for a treat when I got a review copy of her new book, Bonobo Handshake (amazon.com). I could not wait for it to officially come out so I could go to the first public reading (where I took the picture) at the Regulator in Durham on May 27th, on the day of publication.

Vanessa recently moved her blog to a new location on Psychology Today network and had a few interviews in local papers, more sure to come soon.

The book weaves four parallel threads. The first is Vanessa’s own life. Bonobo Handshake starts where ‘Each monkey’ leaves off. And while the ‘Monkey’ covered the period of her life that was pretty distressing, this book begins as her life begins to normalize, describing how she met Brian, fell in love, and got married – a happy trajectory.

The second thread is the science – the experiments they did on behavior and cognition in bonobos and chimps, and how the results fit into the prior knowledge and literature on primate (including human) nature.

The third thread reports on the conservation status of great apes, especially bonobos, and all the social, cultural, financial and political factors that work for or against the efforts to prevent them from going extinct.

The fourth thread is the country of Congo, where all the bonobos in the wild live, especially its recent history of war and its effects on the local people.

The four threads are seamlessly intervowen with each other, but it takes some time into the book to realize that there is, besides the fact that Vanessa was there and did the stuff and wrote about it, another unifying thread – the question of cooperation vs. competition. Vanessa and Brian sometimes love, sometimes fight: what determined one behavior at one time and the opposite at another time?

For the most part, chimps compete and bonobos cooperate: why is that? And what accounts for occasional exceptions to that rule? When threatened, or perceiving to be threatened, animals become insecure. Chimps deal with that insecurity by lashing out – becoming violent and aggressive, or at least putting out a great show of machismo. When bonobos feel insecure (including when they are very young), they solve the problem (and release the tension) by having sex with each other. If chimps won the national elections in the USA, they would probably rule by fear and force, investing mightily into the military, the police and the prison system, going around the world bombing other countries, declaring various internal “Wars on X”, and generally trying to keep the population fearful, subdued and obedient. Bonobos in such a position would always first try to find out a diplomatic solution: how to turn a stranger, or even an enemy into a friend and ally? Share something! Whatever you have: food, shelter, sex…. Everyone is safer that way in the end.

Of course, there are reasons why chimps are one way and bonobos the other. Food is scarce where chimps live, thus there is competition for it, thus the strongest individual wins, and the winner takes all. The position in the hierarchy is the key to survival. Individualism rules. On the other hand, there is plenty of food where bonobos live, enough to share with everyone, eat enough to get bloated, and still plenty left over to just let rot. Why fight over it? Thus, communitarian spirit rules, and if a big strong male starts to feel his oats a little too much, the females will get together and gang up on him as a sisterhood and beat the crap out of him – a rare exception to their usual non-violence, but an act that restores harmony to the group as a whole.

What can we learn from it? That, being equally related to both species, as well as being smarter, we are quite capable of switching between the two modes of reaction to perceived threats: competitive or cooperative. Some people (probably due to the social environment in which they were raised) tend to respond more like chimps, others more like bonobos, but all are capable of behaving both ways. Thus, all are capable of making choices how to react. And the society as a whole can teach people about the exictence of this choice and, in some general ways regarding different kinds of issues, suggest which of the two reactions is condoned by the society and which one will lend you in jail. Studying both chimps and bonobos, comparing them to each other and to humans, can help us understand this choice better, and what it takes to make one or the other reaction to a perceived threat. And even how to study, as researchers, competitions versus cooperation, something that was historically colored by the social upbringing of individual scientists.

[An aside: this is not really relevant to the book as whole, but if I remember correctly it occurs once in the book, and Vanessa sometimes mentions it in her public speaking and on her blog. She mentions the old trope that we are about 98% identical to both chimps and bonobos. That number denotes the identity of sequences of DNA that is expressed in adult, sexually mature individuals at a particular time of year and particular time of day. It ignores all the unexpressed DNA, individual differences, seasonal/daily changes in expression, and effect of the environment. It also ignores the fact that the sequence is not what really matters – it is how the developing organism (from zygote, through embryonic and post-embryonic development, through metamorphosis, growth, maturation, puberty, adulthood and senescence) uses those sequences to effect the development of traits and the day-to-day response of the organism to the environment. It is not the sequence that matters, but which gene is expressed in which cell at what time and in conjunction with which other genes that matters. The number “98% equal” reeks of genetic determinism, which originates with Adaptation and Natural Selection, the 1966 book by George Williams which corrupted generations of biologists, and ‘The Selfish Gene‘, the 1976 book by Richard Dawkins which ruined generations of lay readers and science journalists. It peaked in late 1990s (I wrote this in 1999) with the hype over Human Genome Project (“Holy Grail”, “Blueprint of Life”!) and currently survives only in the realm of that abomination of science we all know as Evolutionary Psychology. There is a lot of literature explaining the poverty of the genocentric and deterministic view of biology, most notably the entire opuses of Stephen Jay Gould and Richard Lewontin, their numerous students and proteges and fans, and an entire generation of evo-devo researchers (the field was spawned/inspired by Gould’s 1977 book ‘Ontogeny and Phylogeny’) and Philosophers of Science (e.g.., Bob Brandon, Bill Wimsatt) who spent some years proving it wrong and, successfully done that, have since moved on to more fertile topics. Actually, one of the easiest-to-read books on the topic for lay audience is titled – What it Means to be 95% Chimpanzee: Apes, People, and their Genes. Saying that humans and bonobos are 98 (or 95, or 99, different numbers are thrown out) percent identical to us is like saying that an airplane and a house are identical because both are built with identical sizes, shapes and colors of Lego blocks – except that one propeller-piece that the airplane has and the house does not. Bonobos and humans are similar because our development is similar, leading to similar phenotypes – not much to do with the sequences of c-DNA libraries. Aside over.]

Conservation of Great Apes depends on humans cooperating to make it happen, but also has to take into account the instrinsic proclivities of different species (chimps, bonobos, gorillas, orangutans and gibbons are all different) towards violence vs. collaboration which dictate the sizes and shapes and organizational schemes of their sanctuaries and eventual wild refuges.

Finally, civil war in Congo is an enormous example of violent competition, but what were its causes? Who chose to compete in this way and why? What was the competition about? Did the end of the Cold War sufficiently weaken the Non-Aligned Movement in a way that reduced the national pride of the people of its member-nations (allowing tribal instincts to take over), reduced the economic cooperation between the member countries (thus sending some of their economies into a downward spiral leading to hopelessness which often leads to lashing out at perceived enemies), or reduced the military cooperation between the members that would scare any potential leader of a tribal movement, or reduced the authority and thus ability of the Movement’s leadership to intervene and prevent wars between the members?

Why did some people come out of war utterly changed – the “living dead” – while others emerged hopeful, energetic and optimistic, full of life and love? How did collaboration of some people help save some of them from murder, and save their psyches from lifelong scars?

Vanessa weaves these four threads expertly and, at the end of the book, you cannot help but care about all four! It is a fast and easy read, you never feel bored or inundated by information, yet you end the book with vastly more knowledge than when you began. And once you know about something enough, you start caring.

I remember as a kid, before the Internet, trying to find something to read after I have finished all 20 library books I took out and still having a couple of weeks of boring vacation ahead of me. Stuck somewhere outside of civilization, with nothing else to do, there was nothing else but to explore the enormous leather-bound classics, each thousands of pages long, each unabridged – stuff that every home has. So I read, slowly and carefully as there was no need to rush, such books as David Copperfield, Pickwick Papers, Teutonic Knights, Moby Dick, Les Miserables, The Road to Life and Martin Eden and others. Being a kid, I did not know anything about any of those topics, and these ancient authors LOVED to write lengthy treateses on various topics over many pages, yet, by getting informed about them, I got to care about Victorian England, Medieval Religious Wars in Poland, classification of whales (and how Melville got it horribly wrong), Paris sewers, educational reforms, and the hard life of becoming a writer. Once, when I contracted something (rubella? scarlet fever?) that made me sick for a couple of days but contagious for another three weeks, with nothing to do at home, I read the unabridged five volumes of War and Peace – at the beginning I did not, but at the end I did care about Russian aristocracy and military strategy (or “how to lose a land war in a Russian winter, part I”).

I don’t know about you, but before I picked up ‘Bonobo Hanshake’ I cared about Vanessa, being a friend, and was thus interested to see what happened after the ‘Monkeys’ book was published. I was interested in bonobo behavior (as we discussed it a lot back in grad school – I did my concentration in Animal Behavior and was a part of the Keck Center for Behavioral Biology) especially as I did not follow the scientific literature on it over the past 6-7 years. I had no idea how endangered bonobos were, nor did I know anything about the civil war in the Congo (and how it is related to the civil war in Rwanda). And while Vanessa did not emulate the 19th century writers, and instead of long chapters on each topic she intertwined brief updates on each of the four threads within each short chapter, I still learned a lot – enough to start caring about the apes, about the people of Congo, about the primatologists working in dangerous places, about individual bonobos and individual Congolese people whose lives intersected Vanessa’s over the past few years. More you know, more you care. So, even if the four themes of this book do not automatically excite you, I suggest you pick up the book – a couple of hours later, you will deeply care about it, know more, want to know even more, and will feel good about it.

Update: In strange synchronicity, Jason Goldman and Brian Switek also reviewed the book today. The book has now also been reviewed by DeLene Beeland, Sheril Kirshenbaum and Christie Wilcox.

Circadian Rhythms in Human Mating

Very brief re-post, from March 18, 2006 – now with a little more added commentary:

I remember from an old review that John Palmer did a study on the diurnal pattern of copulation in humans some years ago. You can see the abstract here.

Now, Roberto Reffinetti repeated the study and published it in the online open-access Journal of Circadian Rhythms here:

The two studies agree: The peak copulatory activity in people living in a modern society is around midnight (or, really, around bedtime) with a smaller secondary peak in the morning around wake-time. This makes sense, as natural (pre-Edison) pattern of human sleep is bi-modal: two bouts of sleep. One bout starts at dusk. The second bout ends at dawn. And there is not much to do for a couple of hours of wakefulness in the middle of the night. You can stand sentry. You can think deep philosophical thoughts. Or, if you are there with your partner…well, you know what to do.

Dig through the papers yourself for additional data on workday-weekend differences and the temporal patterns of the female orgasm.

What is a ‘natural’ sleep pattern?

Nothing too complicated today, but something you should all know (originally from March 13, 2006).

I have mentioned this in my older post: in a natural state, humans do not sleep a long consecutive bout throughout the night (except in the middle of the summer in low latitudes). The natural condition is bimodal – two bouts of sleep interrupted by a short episode of waking in the middle of the night.

In today’s New York Times, there is an article about this:

Sleep Disorder? Wake Up and Smell the Savanna by RICHARD A. FRIEDMAN, M.D.:

————snip———–
Many patients tell me they have a sleep problem because they wake up in the middle of the night for a time, typically 45 minutes to an hour, but fall uneventfully back to sleep. Curiously, there seems to be no consequence to this “problem.” They are unaffected during the day and have plenty of energy and concentration to go about their lives.
————snip———–
The problem, it seems, is not so much with their sleep as it is with a common and mistaken notion about what constitutes a normal night’s sleep.
It’s a question that Dr. Thomas Wehr at the National Institute of Mental Health asked himself in the early 1990’s. He conducted a landmark experiment in which he placed a group of normal volunteers in 14-hour dark periods each day for a month. He let the subjects sleep as much and as long as they wanted during the experiment.
————snip———–
By the fourth week, the subjects slept an average of eight hours a night — but not consecutively. Instead, sleep seemed to be concentrated in two blocks. First, subjects tended to lie awake for one to two hours and then fall quickly asleep. Dr. Wehr found that the abrupt onset of sleep was linked to a spike in the hormone melatonin. Melatonin secretion by the brain’s pineal gland is switched on by darkness.

After an average of three to five hours of solid sleep, the subjects would awaken and spend an hour or two of peaceful wakefulness before a second three- to five-hour sleep period. Such bimodal sleep has been observed in many other animals and also in humans who live in pre-industrial societies lacking artificial light.

Carol Worthman, an anthropologist at Emory University in Atlanta, has studied the sleep patterns of non-Western populations. From the !Kung hunter-gatherers in Africa to the Swat Pathan herders in Pakistan, Dr. Worthman documented a pattern of communal sleep in which individuals drifted in and out of sleep throughout the night.

She speculates that there may even be an evolutionary advantage to interrupted sleep. “When we lived in open exposed savanna, being solidly asleep leaves us vulnerable to predators.”

With artificial light, modern humans have essentially managed to extend their daytime activities late into the night, when all other sensible creatures are busy sleeping.

As a result, we have compressed our natural sleep into artificially short nighttimes, but not all people are so easily tamed by artificial light. Some people, who may just have very strong circadian rhythms, still have this primitive bimodal sleep that they confuse with a sleep disorder.

Add these people to the rest of us who, under the pressures of modern life, often have some trouble falling or staying asleep and there is a large captive audience for drug companies.

Thanks in large part to the meteoric rise in direct-to-consumer advertising, medications like Ambien and Lunesta have become household names and seductive panaceas that millions find hard to resist — even though a majority have no serious sleep problem to repair. If it’s any consolation to those of you who are awake in the middle of the night for an hour or so, reading or watching television, you may simply be the most natural sleepers.

I have nothing to add, except I can also give you an image I dug up – the original data from Wehr’s experiment. See how the sleep is bimodal during the long winter nights and gets compressed during simulated summer:

Related reading:

Everything You Always Wanted To Know About Sleep (But Were Too Afraid To Ask)
Sun Time is the Real Time
Lesson of the Day: Circadian Clocks are HARD to shift!
Seasonal Affective Disorder – The Basics
Are Zombies nocturnal?
Spring Forward, Fall Back – should you watch out tomorrow morning?

Hot Peppers – Why Are They Hot?

I first posted this on July 21, 2006.

Some plants do not want to get eaten. They may grow in places difficult to approach, they may look unappetizing, or they may evolve vile smells. Some have a fuzzy, hairy or sticky surface, others evolve thorns. Animals need to eat those plants to survive and plants need not be eaten by animals to survive, so a co-evolutionary arms-race leads to ever more bizarre adaptations by plants to deter the animals and ever more ingenious adaptations by animals to get around the deterrents.

One of the most efficient ways for a plant to deter a herbivore is to divert one of its existing biochemical pathways to synthesize a novel chemical – something that will give the plant bad taste, induce vomiting or even pain or may be toxic enough to kill the animal.

But there are other kinds of co-evolution between plants and herbivores. Some plants need to have a part eaten – usually the seed – so they can propagate themselves. So, they evolved fruits. The seeds are enveloped in meaty, juicy, tasty packages of pure energy. Those fruits often evolve a sweet smell that can be detected from a distance. And the fruits are often advertised with bright colors – red, orange, yellow, green or purple: “Here I am! Here I am! Please eat me!”

So, the hot peppers are a real evolutionary conundrum. On one hand, they are boldly colored and sweet-smelling fruits – obvious sign of advertising to herbivores. On the other hand, once bitten into, they are far too hot and spicy to be a pleasant experience to the animal. So, what gives?

Back in 1960s, Dan Johnson had an interesting proposal he dubbed “directed deterrence” which suggested that some plants may make choices as to exactly which herbivores to attract and which to deter. Hot peppers are prime candidates for such a phenomenon. What is hot in peppers is capsaicin, a chemical that elicits a sensation of pain when it binds the vanilloid receptors in the nerve endings (usually inside the mouth) of the trigeminal nerve. As it happens, all mammals have capsaicin receptors, but it was found, relatively recently, that birds do not.

To test that hypothesis, Josh Tewksbury used two variants of hot peppers – one very hot (Capsicum annuum) and the other with a mutation that made it not hot at all (Capsicum chacoense) – and offered both as meals to rodents (packrats and cactus mice) and to birds (curve-billed thrashers).

All species ate the sweet kind about equally. When Josh offered them identically prepared meals made out of the hot stuff, the two rodents refused to eat it while the birds happily munched on it.

The study appeared in 2001 in Nature (pdf) and I saw Josh give a talk about it at that time as he was joining our department to postdoc with Dr.Nick Haddad. While my lab-buddy Chris and I gave him a lot of grief in the Q&A session on his lenient criteria of what constitutes a “hungry animal” (he needed them to be hungry for the feeding tests), still the main conclusions of the study are OK.

More importantly, it really happens in nature. Mammals avoid hot peppers out in Arizona where Josh studied them (and made videos of their behavior), but the birds gorged on peppers. When he analyzed the droppings of rodents and birds fed peppers, he saw that seeds that passed through avian intestinal tracts were fully fertile, while seeds eaten by mammals were chewed, crushed, broken or semi-digested and not fertile at all.

Additionally, the thrashers tend to spend a lot of time on fruiting shrubs of different kinds. While there, they poop. The hot pepper seeds in the droppings germinate right there and this is an ideal shady spot for them to grow.

What a great example of a (co)evolutionary adaptation!

Related: Hot Peppers

Let’s Talk About Evolution [Video]

No need for me to add anything – just watch it and share:

BIO101 – Introduction to Anatomy and Physiology

In this lecture, as well as in the previous one and the next one, I tackle areas of Biology where I am really weak: origin of life, diversity of life, and taxonomy/systematics. These are also areas where there has been a lot of change recently (often not yet incorporated into textbooks), and I am unlikely to be up-to-date, so please help me bring these lectures up to standards…. This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

———————————————

Anatomy is the sub-discipline of biology that studies the structure of the body. It describes (and labels in Latin) the morphology of the body: shape, size, color and position of various body parts, with particular attention to the internal organs, as visible by the naked eye. Histology is a subset of anatomy that describes what can be seen only under the microscope: how cells are organized into tissues and tissues into organs. (Classical) embryology describes the way tissues and organs change their shape, size, color and position during development.

Anatomy provides the map and the tools for the study of the function of organs in the body. It describes (but does not explain) the structure of the body. Physiology further describes how the body functions, while evolutionary biology provides the explanation of the structure and the function.

While details of human anatomy are essential in the education of physicians and nurses (and animal anatomy for veterinarians), we do not have time, nor do we need to pay too much attention to fine anatomical detail. We will pick up on relevant anatomy as we discuss the function of organs: physiology.

There are traditionally two ways to study (and teach) physiology. The first approach is medical/biochemical. The body is subdivided into organ systems (e.g., respiratory, digestive, circulatory, etc.) and each system is studied separately, starting with the physiology of the whole organism and gradually going down to the level of organs, tissues, cells and molecules, ending with the biochemistry of the physiological function. Only the human body is studied. Often, pathologies and disorders are used to illustrate how organs work – just like fixing a car engine by replacing a broken part helps us understand how the engine normally works, so studying diseases helps us understand how the healthy human body works.

The other approach is ecological/energetic. The physiological functions are divided not by organ system, but by the problem – imposed by the environment – that the body needs to solve in order to survive and reproduce, e.g., the problem of thermoregulation (body temperature), osmoregulation (salt/water balance), locomotion (movement), stress response, etc., each problem utilizing multiple organ systems. Important aspect of this approach is the study of the way the body utilizes energy: is the solution energetically optimal? Individuals that have solved a problem with a more energy-efficient physiological mechanism will be favored by natural selection – thus this approach is also deeply rooted in an evolutionary context. Finally, this approach is very comparative – study of animals that live in particularly unusual or harsh environments helps us understand the origin and evolution of physiological mechanisms both in humans and in other animals.

The textbook is unusually good (for an Introductory Biology textbook) in trying to bridge and combine both approaches. Unfortunately, we do not have enough time to cover all of the systems and all of the problems in detail, so we will stick to the first, medical approach and cover just a few of the systems of the human body, but I urge you to read the relevant textbook chapters in order to understand the ecological and evolutionary aspects of physiology as well (not to mention some really cool examples of problem-solving by animal bodies). Hint: use the “Self Test” questions at the end of each chapter and if you answer them correctly, you are ready for the exam.

Let’s start out by looking at a couple of important basic principles that pertain to all of physiology. One such principle is that of scaling, for which you should read the handout that we will discuss in class next time. The second important principle in physiology is the phenomenon of feedback loops: both negative and positive feedback loops.

Negative feedback loop works in a way very similar to the graph we drew when we discussed behavior. The body has a Sensor that monitors the state of the body – the internal environment (as opposed to external environment we talked about when discussing behavior), e.g,. the blood levels of oxygen and carbon dioxide, blood pressure, tension in the muscles, etc. If something in the internal environment changes from the normal, optimal values, the sensor informs the Integrator (usually the nervous system) which initiates action (via an Effector) to bring back the body back to its normal state.

Thus, an event A leads to response B which leads to the countering and elimination of the event A. Almost every function in the body operates like a negative feedback loop. For instance, if a hormone is secreted, along with the functional effect of that hormone, there will also be a trigger of a negative feedback loop that will stop the further secretion of that hormone.

There are very few functions in the body that follow a different pattern – the positive feedback loop. There, an event A leads to response B which leads to re-initiation and intensification of the event A which leads to a stronger response B…and so on, until a threshold is reached or the final goal is accomplished, when everything goes abruptly back to normal.

We will take a look at an example of the positive feedback loop that happens in the nervous system next week. For now, let’s list some other notable positive feedback loops in humans.

First, the blood clotting mechanism is a cascade of biochemical reactions that operates according to this principle. An injury stimulates production of a molecule that triggers production of another molecule which triggers production of another molecule as well as production of more of the first molecule, and so on, until the injury has completely closed.

Childbirth is another example of the positive feedback loop. When the baby is ready to go out (and there’s no stopping it at this point!), it releases a hormone that triggers the first contraction of the uterus. The contraction of the uterus pushes the baby out a little. That movement of the baby stretches the wall of the uterus. The wall of the uterus contains stretch receptors which send signals to the brain. In response to the signal, the brain (actually the posterior portion of the pituitary gland, which is an outgrowth of the brain) releases hormone oxytocin. Oxytocin gets into the bloodstream and reaches the uterus triggering the next contraction which, in turn, moves the baby which further stretches the wall of the uterus, which results in more release of oxytocin…and so on, until the baby is expelled, when everything returns to normal.

Next example of the positive feedback loop is also related to babies – nursing. When the infant is hungry, mother brings its mouth to the nipple of the breast. When the baby latches onto the nipple and tries to suck, this stimulates the receptors in the nipple which notify the brain. The brain releases hormone oxytocin from the posterior pituitary gland. Oxytocin gets into the bloodstream and stimulates the mammary gland to release milk (not to synthesize milk – it is already stored in the breasts). Release of milk at the nipple stimulates the baby to start suckling vigorously, which stimulates the receptors in the nipple even more, so there is even more oxytocin released from the pituitary and even more milk is released by the mammary gland, and so on, until the baby is satiated and unlatches from the breast, when everything goes back to normal.

Next example of the positive feedback loop is also related to babies, but nine months earlier. Copulation – yes, having sex – is an example of a positive feedback loop, both in females and in males. Initial stimulation of the genitals stimulates the touch receptors which notify the brain which, in turn, stimulates continuation (and gradual speeding up) of movement, which provides further tactile stimulation, and so on, until the orgasm, after which everything goes back to normal (afterglow notwithstanding).

The last example also applies to the nether regions of the body. Micturition (urination) is also a positive feedback loop. The wall of the urinary bladder is built in such a way that there are several layers of cells. As the bladder fills up, the wall stretches and these cells move around until the wall is only a single cell thick. At this point, urination is inevitable (cannot be stopped by voluntary control). Beginning of the urination starts the movement of the cells back from single-layer state to multi-layer state. This contracts the bladder further which forces urine out even more which contracts the wall of the bladder even more, and so on until the bladder is completely empty again and everything goes back to normal.

The concept of feedback loops is essential for the understanding of the principle of homeostasis. Homeostatic mechanisms ensure that the internal environment remains constant and all the parameters are kept at their optimal levels (e.g,. temperature, pH, salt/water balance, etc) over time. If a change in the environment (e.g., exposure to heat or cold) results in the change of internal body temperature, this is sensed by thermoreceptors in the body. This triggers corrective mechanisms: if the body is overheated, the capillaries in the skin expand and radiate heat and the sweat gland release sweat; if the body is too cold, the capillaries in the skin contract, the muscles start shivering, the hairs stand up (goosebumps), and the thyroid hormones are released, resulting in opening of pores in the membranes of mitochondria in the muscles, thus reducing the efficiency of the break-down of glucose to water and carbon-dioxide, thus producing excess heat. Either way, the body temperature will be returned to its optimal level (around 37 degrees Celsius), which is called the set-point for body temperature. Each aspect of the internal environment has its own set-point which is defended by homeostatic mechanisms.

While essentially correct, there is a problem with the concept of homeostasis. One of the problems with the term “homeostasis” is linguistic: the very term homeostasis is misleading. “Homeo” means ‘similar, same’ and “stasis” means ‘stability’. Thus, the word homeostasis (coined by Walter Cannon in the early 20th century) suggests strong and absolute constancy. Imagine that you were told to draw a graphical representation of the concept of homeostasis in 10 seconds. Without sufficient time to think, you would probably draw something like this:

The main characteristic of this graph is that the set-point is constant over time. But that is not how it works in the real world. The graph above is correct only if the time-scale (on the X-axis) spans only seconds to minutes. If it is expanded to hours, days or years, the graph would be erroneous – the line would not be straight and horizontal any more. The set point changes in a predictable and well-controlled manner. For instance, the set-point for testosterone levels in the blood in human males over the course of a lifetime may look like this:

That would be an example of developmental control of a set-point. At each point in time, that set-point is defended by homeostatic mechanisms, but the set-point value is itself controlled by other physiological processes. Another example of controlled change of a set-point may look like this:

This would be an example of an oscillatory control of a set-point. In the early 1980s, Nicholas Mrosovsky coined a new term to replace ‘homeostasis’ and specifically to denote controlled changes in set-points of all biochemical, physiological and behavioral values – rheostasis.

Almost every aspect of physiology (and behavior) exhibits rheostasis, both developmental and oscillatory (daily and/or yearly rhythms). Some notable exceptions are blood pH (which has to be kept within very narrow range 7.35-7.45) and blood levels of Calcium. If pH or Calcium levels move too far away from the optimal value, cells in the body (most notably nerve cells, muscles and heart cells) cannot function properly and the body is in danger of immediate death.

Additional Readings:

‘Medicine Needs Evolution’ by Nesse, Stearns and Omenn

Previously in this series:

BIO101 – Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype
BIO101 – From Genes To Species: A Primer on Evolution
BIO101 – What Creatures Do: Animal Behavior
BIO101 – Organisms In Time and Space: Ecology
BIO101 – Origin of Biological Diversity
BIO101 – Evolution of Biological Diversity
BIO101 – Current Biological Diversity

Spring Forward, Fall Back – should you watch out tomorrow morning?

I originally published this on November 2, 2008. You really need to reed the comments there, at the original post, as well as the “related” posts at the bottom of this post, as this story had some legs – a lot of discussion ensued.

If you live in (most places in) the United States as well as many other countries, you have reset your clocks back by one hour last night (or last week). How will that affect you and other people?

One possibility is that you are less likely to suffer a heart attack tomorrow morning than on any other Monday of the year. Why? Let me try to explain in as simple way as possible (hoping that oversimplification will not lead to intolerable degrees of inaccuracy).

Almost all biochemical, physiological and behavioral parameters in almost all (at least multicellular) organisms display diurnal (daily) rhythms and most of those are directly driven by the circadian clock (or, more properly, by the circadian system). Here is an old and famous chart displaying some of the peaks (acrophases) of various physiological functions in the human:

It may be a little fuzzy, but you can see that most of the peaks associated with the cardiovascular function are located in the afternoon. The acrophases you see late at night are for things like “duration of systole” and “duration of diastole” which means that the Heart Rate is slow during the night. Likewise, blood pressure is low during the night while we are asleep.

Around dawn, heart rate and blood pressure gradually rise. This is a direct result of the circadian clock driving the gradual rise in plasma epinephrine and cortisol. All four of those parameters (HR, BP, Epinephrine and Cortisol) rise roughly simultaneously at dawn and reach a mini-peak in the morning, at the time when we spontaneously wake up:

This rise prepares the body for awakening. After waking up, the heart parameters level off somewhat and then very slowly rise throughout the day until reaching their peak in the late afternoon.

Since the four curves tend to be similar and simultaneous in most cases in healthy humans, let’s make it easier and clearer to observe changes by focusing only on the Cortisol curve in the morning, with the understanding that the heart will respond to this with the simultaneous rise in heart rate and blood pressure. . This is how it looks on a day when we allow ourselves to wake up spontaneously:

But many of us do not have the luxury of waking up spontaneously every day. We use alarm clocks instead. If we set the alarm clock every day to exactly the same time (even on weekends), our circadian system will, in most cases (more likely in urban than rural areas, though), entrain to the daily Zeitgeber – the ring of the alarm-clock – with a particular phase-relationship. This usually means that the rise in cardiovascular parameters will start before the alarm, but will not quite yet reach the peak as in spontaneous awakening:

The problem is, many of us do not set the alarm clocks during the weekend. We let ourselves awake spontaneously on Saturday and Sunday, which allows our circadian clock to start drifting – slowly phase-delaying (because for most of us the freerunning period is somewhat longer than 24 hours). Thus, on Monday, when the alarm clock rings, the gradual rise of cortisol, heart rate and blood pressure will not yet be as far along as the previous week. The ring of the alarm clock will start the process of resetting of the circadian clock – but that is the long-term effect (may take a couple of days to complete, or longer.).

The short term effect is more dramatic – the ring of the alarm clock is an environmental stressor. As a result, epinephrine and cortisol (the two stress hormones) will immediately and dramatically shoot up, resulting in an instantaneous sharp rise in blood pressure and heart rate. And this sharp rise in cardiovascular parameters, if the heart is already damaged, can lead to a heart attack. This explains two facts: 1) that heart attacks happen more often on Mondays than other days of the week, and 2) that heart attacks happen more often in the morning, at the time of waking up, than at other times of day:

Now let’s see what happens tomorrow, the day after the time-change. Over the weekend, while you were sleeping in, your circadian system drifted a little, phase delaying by about 20 minutes on average (keep in mind that this is an average – there is a vast variation in the numerical value of the human freerunning circadian period). Thus, your cardiovascular parameters start rising about 20 minutes later tomorrow morning than last week. But, your alarm clock will ring an entire hour later than last week – giving you an average of a 40-minute advantage. Your heart will be better prepared for the stress of hearing the ringing than on any other Monday during the year:

Now let’s fast-forward another six month to the Spring Forward weekend some time in March or April of next year. Your circadian system delays about 20 minutes during the weekend. On top of that, your alarm clock will ring an hour earlier on that Monday than the week before. Thus, your cardiovascular system is even further behind (80 minutes) than usual. The effect of the stress of the alarm will be thus greater – the rise in BP and HR will be even faster and larger than usual. Thus, if your heart is already damaged in some way, your chances of suffering an infarct are greater on that Monday than on any other day of the year:

This is what circadian theory suggests – the greater number of heart attacks on Mondays than other days of the week (lowest during the weekend), the greatest number of heart attacks on the Monday following the Spring Forward time-change compared to other Mondays, and the lowest incidence of heart attacks on the Monday following the Fall Back time-change compared to other Mondays.

A couple of days ago, a short paper appeared that tested that theoretical prediction and found it exactly correct (Imre Janszky and Rickard Ljung, October 30, 2008, Shifts to and from Daylight Saving Time and Incidence of Myocardial Infarction, The New England Journal of Medicine, Volume 359:1966-1968, Number 18.). The authors looked at a large dataset of heart attacks in Sweden over a large period of time and saw that (if you look at the numbers) the greatest number of heart attacks happens on Mondays compared to other days of the week (and yes, the numbers are lowest during the weekend), the greatest number of heart attacks occur on the Monday following the Spring Forward time-change compared to Mondays two weeks before and after, and the lowest incidence of heart attacks happens on the Monday following the Fall Back time-change compared to Mondays two weeks before and after:

Thus, the predictions from the circadian theory were completely and clearly correct. But I was jarred by the conclusions that the authors drew from the data. They write:

The most plausible explanation for our findings is the adverse effect of sleep deprivation on cardiovascular health. According to experimental studies, this adverse effect includes the predominance of sympathetic activity and an increase in proinflammatory cytokine levels.3,4 Our data suggest that vulnerable people might benefit from avoiding sudden changes in their biologic rhythms.

It has been postulated that people in Western societies are chronically sleep deprived, since the average sleep duration decreased from 9.0 to 7.5 hours during the 20th century.4 Therefore, it is important to examine whether we can achieve beneficial effects with prolonged sleep. The finding that the possibility of additional sleep seems to be protective on the first workday after the autumn shift is intriguing. Monday is the day of the week associated with the highest risk of acute myocardial infarction, with the mental stress of starting a new workweek and the increase in activity suggested as an explanation.5 Our results raise the possibility that there is another, sleep-related component in the excess incidence of acute myocardial infarction on Monday. Sleep-diary studies suggest that bedtimes and wake-up times are usually later on weekend days than on weekdays; the earlier wake-up times on the first workday of the week and the consequent minor sleep deprivation can be hypothesized to have an adverse cardiovascular effect in some people. This effect would be less pronounced with the transition out of daylight saving time, since it allows for additional sleep. Studies are warranted to examine the possibility that a more stable weekly pattern of waking up in the morning and going to sleep at night or a somewhat later wake-up time on Monday might prevent some acute myocardial infarctions.

And in the quotes in the press release they say the same thing, so it is not a coincidence:

“It’s always been thought that it’s mainly due to an increase in stress ahead of the new working week,” says Dr Janszky. “But perhaps it’s also got something to do with the sleep disruption caused by the change in diurnal rhythm at the weekend.”

Dr.Isis has already noted this and drew the correct conclusion. She then goes on to say something that is right on the mark:

And, of course, my first thought is, what about all the other times we are sleep deprived by, you know, one hour. Is waking up in the middle of the night to feed Baby Isis potentially going to cause Dr. Isis to meet her maker early? In that case Baby Isis can freakin’ starve. But, this is the New England Journal of Medicine and Dr. Isis appreciates the innate need that authors who publish here have to include some clinical applicability in their work.

The authors responded to Dr.Isis in the comments on her blog and said, among else:

We wonder whether you have ever tried to publish a research letter somewhere. The number of citations (maximum 5!) and the number of words are strictly limited. Of course we are familiar with studies on circadian rhythms and cardiovascular physiology. There was simply no space to talk more about biological rhythms than we actually did.

But what they wrote betrays that even if they are familiar with the circadian literature, they do not really understand it. Nobody with any circadian background ever speculates about people’s conscious expectations of a stressful week as a cause of heart attacks on Monday mornings. Let me try to explain why I disagree with them on two points they raise (one of which I disagree with more strongly than the other).

1) Sleep Deprivation. It is important to clearly distinguish between the acute and the chronic sleep deprivation. Sleepiness at any given time of day is determined by two processes: a homeostatic drive that depends on the amount of sleep one had over a previous time period, and a circadian gating of sleepiness, i.e., at which time of day is one most likely to fall asleep. Sleep deprivation affects only the homeostatic drive and has nothing to do with circadian timing.

Humans, like most other animals, are tremendously flexible and resilient concerning acute sleep deprivation. Most of us had done all-nighters studying for exams, or partying all night with non ill effects – you just sleep off the sleep debt the next day or the next weekend and you are fine. Dr.Isis is not going to die because her baby wakes her up several times during the night. This is all part of a normal human ecology, and human physiology had adapted to such day-to-day variations in opportunities for sleep.

The Chronic sleep deprivation is a different animal altogether. This means that you are getting less sleep than you need day after day, week after week, month after month, year after year, with rarely or never sleeping off your sleep debt (“catching up on sleep”). As a result, your cognitive functions suffer. If you are a student, you will have difficulties understanding and retaining the material. If you are a part of the “creative class”, you will be less creative. If you are a scientist, you may be less able to clearly think through all your experiments, your data, and your conclusions. No matter what job you do, you will make more errors. You may suffer microsleep episodes while driving and die in a car wreck. Your immune system will be compromised so you will constantly have sniffles and colds, and may be more susceptible to other diseases.

And yes, a long term chronic sleep deprivation may eventually damage your heart to the extent that you are more susceptible to a heart attack. This means that you are more likely to suffer a heart attack, but has no influence on the timing of the heart attack – it is the misalignment between the natural circadian rhythms of your body and the social rhythms imposed via a very harsh stressor – the alarm clock – that determines the timing. Being sleep deprived over many years means you are more likely to have a heart attack, but cannot determine when. Losing just one hour of sleep will certainly have no effect at all.

Thus, the data presented in the paper have nothing to say about sleep deprivation.

2) Cytokines. These are small molecules involved in intercellular signaling in the immune system. Like everything else, they are synthesized in a diurnal manner. But they act slowly. Maybe they play some small part in the gradual damage of the heart in certain conditions (prolonged inflammation, for instance), thus they may, perhaps, have a role in increasing risk of a heart attack. But they play no role in timing of it. Thus they cannot be a causal factor in the data presented in the paper which are ONLY about timing, not the underlying causes. The data say nothing as to who will suffer a heart attack and why, only when you will suffer one if you do.

If I was commissioned to write a comprehensive review of sleep deprivation, I may have to force myself to wade through the frustratingly complicated and ambiguous literature on cytokines in order to write a short paragraphs under a subheading somewhere on the 27th page of the review.

If I had a severe word-limit and needed to present the data they showed in this paper, I would not waste the space by mentioning the word “cytokine” at all (frankly, that would not even cross my mind to do) as it is way down the list of potential causes of heart attack in general and has nothing to do with the timing of heart attacks at all, thus irrelevant to this paper.

So, it is nice they did the study. It confirms and puts clear numbers on what “everybody already knew for decades” in the circadian community. But their interpretation of the data was incorrect. This was a purely chronobiological study, yet they chose to present it as a part of their own pet project instead and tried mightily to make some kind of a connection to their favourite molecules, the cytokines, although nothing warranted that connection. Nails: meet hammer.

The fake-insulted, haughty and inappropriate way/tone they responded to Dr.Isis is something that is important to me professionally, as is there misunderstanding of both the role and the tone of science blogs, so I will revisit that issue in a separate post later. I promise. It is important.

But back to Daylight Saving Time. First, let me ask you (again) to see Larry’s post from last year, where you will find a lot of useful information and links about it. What is important to keep in mind is that DST itself is not the problem – it is the time-changes twice a year that are really troubling.

Another important thing to keep in mind is that DST was instituted in the past at the time when the world looked very different. At the time when a tiny sliver of the population is still involved in (quite automated and mechanized) agriculture, when electricity is used much more for other things than illumination (not to mention that even the simple incandescent light bulbs today are much more energy efficient than they used to be in the past, not to mention all the newfangled super-efficient light-bulbs available today), when many more people are working second and third shifts than before, when many more people work according to their own schedules – the whole idea of DST makes no sense any more.

Even if initially DST saved the economy some energy (and that is questionable), it certainly does not do so any more. And the social cost of traffic accidents and heart attacks is now much greater than any energy savings that theoretically we may save.

Furthermore, it now seems that circadian clocks are harder to shift than we thought in the past. Even that one-hour change may take some weeks to adjust to, as it is not just a singular clock but a system – the main pacemaker in the SCN may shift in a couple of days, but the entire system will be un-synchronized for some time as it may take several weeks for the peripheral clocks in the liver and intestine to catch up – leading to greater potential for other disorders, e.g., stomach ulcers.

The social clues (including the alarm clocks) may not be as good entraining agents as we thought before either, especially in rural areas where the natural lighting still has a profound effect.

Finally, the two time-change days of the year hit especially hard people with Bipolar Disorder and with Seasonal Affective Disorder – not such a small minority put together, and certainly not worth whatever positives one may find in the concept of DST. We should pick one time and stick with it. It is the shifts that cost the society much more than any potential benefits of DST.

Related reading:

Roosevelts on Toilets
The Shock Value of Science Blogs
Add yet another factor to the circadian hypothesis of morning heart-attacks
Daylight Saving Time
Daylight Savings Time worse than previously thought
Time
Sun Time is the Real Time
Lesson of the Day: Circadian Clocks are HARD to shift!
Everything You Always Wanted To Know About Sleep (But Were Too Afraid To Ask)
Seasonal Affective Disorder – The Basics
Circadian clock without DNA–History and the power of metaphor
Lithium, Circadian Clocks and Bipolar Disorder
Are Zombies nocturnal?
Diversity of insect circadian clocks – the story of the Monarch butterfly
Me and the copperheads–or why we still don’t know if snakes secrete melatonin at night
The Mighty Ant-Lion
City Of Light: Insomniac Urban Animals

Sun Time is the Real Time

I originally published this on January 31, 2007.

If you really read this blog “for the articles”, especially the chronobiology articles, you are aware that the light-dark cycle is the most powerful environmental cue entraining circadian clocks. But it is not the only one. Clocks can also be entrained by a host of other (“non-photic”) cues, e.g., scheduled meals, scheduled exercise, daily dose of melatonin, etc.

Clocks in heterothermic (“cold-blooded”) animals can also entrain to temperature cycles. Lizards can entrain to temperature cycles (pdf) in which the difference between nightime low and daytime high temperatures is as small as 2 degrees Celsius. When taken out of a warm-blooded animal, the SCN clock can also be entrained (if you are a regular here, you recognize the name, don’t you) by temperature cycles (presumably a nice feedback loop that stabilizes the mammalian rhythms: the clock entrains body temperature cycles and body temperature cycles entrain the clock).

Some rodents can phase-shift (and thus presumably entrain if presented daily) their clocks under the influence of conspecifics odors or pheromones. In an old study (which was not very good, but enough can be concluded from the data), rats held in groups in constant conditions entrained their rhythms to each other (while the quail did not), suggesting some kind of social entrainment, perhaps mediated by smell.

Social animals are supposed to be sensitive to social cues and it is presumed that their clocks can be entrained by social cues as well. It is also widely believed that no other animal’s clock is as sensitive to social cues as the human’s.

Everyone who’s been in this field has heard the anecdotes about the experiments conducted by Jurgen Asschoff and others at Andechs, Germany in the 1950s and 60s, in which human volunteers were kept in constant light conditions for prolonged periods of time in old underground bunkers (I think Asschoff’s bunkers are now preserved as monuments to science, just like the Knut Schmidt-Nielsen’s camel chamber is preserved over at Duke University with a nice brass plaque). According to the lore of the field (were those things ever published?), social cues like newspapers, or physical appearance of technicians called in to bring in the food (e.g., sleepy look, or the 5-o-clock stubble) were sufficient cues to entrain human subjects.

It is always difficult to directly test the relative importance of different environmental cues. Sure, one can put them in direct competition by having, for instance, a light-dark cycle and a temperature cycle being 180 degrees out of phase and see to which one of those animals actually entrain (such a study in Neurospora was published a few years back). But, how do you know that the intensities are equivalent? What is the equivalent of 1000 lux in degrees Celsius? Ten, twenty, a hundred?

So, perhaps one should look at the ecologicaly relevant levels of intensity of environmental cues. But how does one dissociate two synchronous cues out in nature in order to do the experiment? Well, of course, use humans for this experiment as the society has already made sure some cues get dissociated! And that is exactly what Till Roenneberg, C. Jairaj Kumar and Martha Merrow did in a new paper in Current Biology: The human circadian clock entrains to sun time (Volume 17, Issue 2 , 23 January 2007, Pages R44-R45)

What they did is take advantage of the fact that time zones are very broad – about 15 angle degrees each. This means that the official (social) midnight and the real (geophysical) midnight coincide only in a very narrow strip running smack through the middle of the time zone. Most of Europe is one time zone. If it is officially midnight in Europe, i.e., the clock strikes 12, it is really midnight (as in “Mid-Night”) in a place like Munich, but it is already something like an hour later in Bucharest, and still something like an hour to wait for it in Lisbon.

So, in this paper, they looked at actual entrainment patterns of more than 21000 Germans to see if they entrain to the real midnight – suggesting that light cues are stronger, or to official midnight, suggesting that social cues are stronger. They controlled for age, sex, chronotype (owls/larks) and general culture (former East and West Germanies) and what they found was very interesting: in small cities, towns and villages, people entrain to the light-dark cycles and mostly ignore the official time. However, bigger the city, more independent the entrainment was from the real light-dark cycle. The phase was delayed and more in sync with the official time.

It is hard to interpret the findings, really. Do people in big cities entrain to official time due to stronger social cues (the busy big-city life and social scene) or because they are better sheltered from the natural light-dark cycle and, due to all the light pollution and technology, better able to impose on their clocks an artificial light-dark cycle. I am assuming that untangling this question is going to be their next project.

But, one thing this study did was make us take a more skeptical look at all those Andech bunkers anecdotes. Sure, social cues may work in the absence of all other cues, but they are not THAT powerful and do not seem to be able to overcome the effects of natural light cycles in places in which people are able to perceive a natural light cycle. I guess one can view the life in a big city (“black box”) as being in a laboratory experiment in which the society acts as an experimenter, imposing the light-dark cycle on people, while the life out in the country is more like a field experiment in which the human subjects are exposed to the natural environmental cues.

Addendum

Related:

Sun Time is the Real Time
Lesson of the Day: Circadian Clocks are HARD to shift!
Everything You Always Wanted To Know About Sleep (But Were Too Afraid To Ask)
Seasonal Affective Disorder – The Basics
Circadian clock without DNA–History and the power of metaphor
Are Zombies nocturnal?
Diversity of insect circadian clocks – the story of the Monarch butterfly
Me and the copperheads–or why we still don’t know if snakes secrete melatonin at night
The Mighty Ant-Lion
City Of Light: Insomniac Urban Animals

Are Zombies nocturnal?

For Halloween, I thought I’d republish this old post of mine from July 1, 2010.

Blame ‘Night of the Living Dead’ for this, but many people mistakenly think that zombies are nocturnal, going around their business of walking around town with stilted gaits, looking for people whose brains they can eat, only at night.

You think you are safe during the day? You are dangerously wrong!

Zombies are on the prowl at all times of day and night! They are not nocturnal, they are arrhythmic! And insomniac. They never sleep!

Remember how one becomes a zombie in the first place? Through death, or Intercision, or, since this is a science blog and we need to explain this scientifically, through the effects of tetrodotoxin. In any case, the process incurs some permanent brain damage.

One of the brain centers that is thus permanently damaged is the circadian clock. But importantly, it is not just not ticking any more, it is in a permanent “day” state. What does that mean practically?

When the clock is in its “day” phase, it is very difficult to fall asleep. Thus insomnia.

When the clock is in its “day” phase, metabolism is high (higher than at night), thus zombies require a lot of energy all the time and quickly burn through all of it. Thus constant hunger for high-calory foods, like brains.

Insomnia, in turn, affects some hormones, like ghrelin and leptin, which control appetite. If you have a sleepless night or chronic insomnia, you also tend to eat more at night.

But at night the digestive function is high. As zombies’ clock is in the day state, their digestion is not as efficient. They have huge appetite, they eat a lot, but they do not digest it well, and what they digest they immediately burn. Which explains why they tend not to get fat, while living humans with insomnia do.

Finally, they have problems with wounds, you may have noticed. Healing of wounds requires growth hormone. But growth hormone is secreted only during sleep (actually, during slow sleep phases) and is likewise affected by ghrelin.

In short, a lot of the zombies’ physiology and behavior can be traced back to their loss of circadian function and having their clock being in a permanent “day” state.

But the real take-home message of this is…. don’t let your guard down during the day!


Picture of me as a Zombie drawn by Joseph Hewitt of Ataraxia Theatre whose latest project, GearHead RPG, is a sci-fi rogue-like game with giant robots and a random story generator – check it out.

Revenge of the Zombifying Wasp

As it is Halloween, I am republishing my old post (from February 04, 2006, reposted on July 1, 2010):

Ampulex compressa

I was quite surprised that Carl Zimmer, in research for his book Parasite Rex, did not encounter the fascinating case of the Ampulex compressa (Emerald Cockroach Wasp) and its prey/host the American Cockroach (Periplaneta americana, see also comments on Aetiology and Ocellated).

In 1999, I went to Oxford, UK, to the inaugural Gordon Conference in Neuroethology and one of the many exciting speakers I was looking forward to seeing was Fred Libersat. The talk was half-hot half-cold. To be precise, the first half was hot and the second half was not.

In the first half, he not just introduced the whole behavior, he also showed us a longish movie, showing in high magnification and high resolution all steps of this complex behavior (you can see a cool picture of the wasp’s head here).

How the wasp injects the cockroach

First, the wasp gives the roach a quick hit-and-run stab with its stinger into the body (thorax) and flies away. After a while, the roach starts grooming itself furiously for some time, followed by complete stillness. Once the roach becomes still, the wasp comes back, positions itself quite carefully on top of the raoch and injects its venom very precisely into the subesophageal ganglion in the head of the roach. The venom is a cocktail of dopamine and protein toxins so the effect is behavioral modification instead of paralysis.

Apparently, the wasp’s stinger has receptors that guide it to its precise target:

“To investigate what guides the sting, Ram Gal and Frederic Libersat of Ben-Gurion University in Beer-Sheva, Israel, first introduced the wasp to roaches whose brains had been removed. Normally, it takes about a minute for the wasp to find its target, sting, and fly off. But in the brainless roaches, the wasps searched the empty head cavity for an average of 10 minutes. A radioactive tracer injected into the wasps revealed that when they finally did sting, they used about 1/6 the usual amount of venom. The wasps knew something was amiss.”

The wasp then saws off the tips of the roach’s antennae and drinks the haemolymph from them. It builds a nest – just a little funnel made of soil and pebbles and leads the roach, by pulling at its antenna as if it was a dog-leash, into the funnel. It then lays an egg onto the leg of the roach, closes off the entrance to the funnel with a rock and leaves. The roach remains alive, but completely still in the nest for quite some time (around five weeks). The venom, apart from eliminating all defense behaviors of the roach, also slows the metabolism of the cockroach, allowing it to live longer without food and water. After a while, the wasp egg hatches, eats its way into the body of the roach, eats the internal organs of the roach, then pupates and hatches. What comes out of the (now dead) cockroach is not a larva (as usually happens with insect parasitoids) but an adult wasp, ready to mate and deposit eggs on new cockroaches.

Why was the second half of the talk a disappointment? I know for a fact I was not the only one there who expected a deeper look into evolutionary aspects of this highly complex set of behaviors. However, the talk went into a different direction – interesting in itself, for sure, but not as much as an evolutionary story would have been. Libersat described in nitty-gritty detail experiments that uncovered, one by one, secrets of the neuroanatomy, neurophysiology and neurochemistry of the cockroach escape behavior – the one suppressed by toxin – as well as the chemistry of the toxin cocktail. Ganglion after ganglion, neuron after neuron, neurotransmitter after neurotransmitter, the whole behavior was charted for us on the screen. An impressive feat, but disappointing when we were all salivating at a prospect of a cool evolutionary story.

He did not say, for instance, what is the geographic overlap between the two species. I had to look it up myself afterwards. American cockroach can be found pretty much everywhere in the world. The wasp also has a broad geographical range from Africa to New Caledonia (located almost directly between Australia and Fiji) and, since 1941, Hawaii (another example of a non-native species wreaking havoc on the islands), but not everywhere in the world, especially not outside the tropics – there are most definitely parts of the planet where there are roaches but no Ampulex compressa.

In most cases in which one species is susceptible to the venom or toxin of another species, the populations which share the geography are also engaged in an evolutionary arms-race. The victim of the venom evolves both behavioral defenses against the attack of the other species and biochemical resistance to the venom. In turn, the venom evolves to be more and more potent and the animal more and more sneaky or camouflaged or fast in order to bypass behavioral defenses.

There are many examples of such evolutionary arms-races in which one of the species is venomous/toxic and the other one evolves resistance. For instance, garter snakes on the West Coast like to eat rough-side newts. But these newts secrete tetrodotoxin in their skins. The predator is not venomous, but it has to deal with dangerous prey. Thus, in sympatry (in places where the two species co-exist) snakes have evolved a different version of a sodium channel. This version makes the channel less susceptible to tetrodotoxin, but there is a downside – the snake is slower and more lethargic overall. In the same region, the salamanders appear to be evolving ever more potent skin toxin cocktails.

Similar examples are those of desert ground squirrels and rattlesnakes (both behavioral and biochemical innovations in squirrels), desert mice (Southwest USA) and scorpions (again it is the prey which is venomous), and honeybees and Death’s-Head sphinx-moths (moths come into the hives and steal honey and get stung by bees after a while).

But Libersat never wondered if cockroaches in sympatry with Emerald wasps evolved any type of resistance, either behavioral or physiological. Perhaps the overwhelming number of roaches in comparison with the wasps makes any selective pressure too weak for evolution of defenses. But that needs to be tested. He also never stated if the attack by the wasp happens during the day or during the night. Roaches are nocturnal and shy away from light. The movie he showed was from the lab under full illumination. Is it more difficult for the wasp to find and attack the roach at night? Is it more difficult for the roach to run away or defend itself during the day? Those questions need to be asked.

Another piece of information that is missing is a survey of parasitizing behaviors of species of wasps most closely related to Ampulex compressa. Can we identify, or at least speculate about, the steps in the evolution of this complex set of behaviors (and the venom itself)? What is the precursor of this behavior: laying eggs on found roach carcasses, killing roaches before laying eggs on their carcasses, laying eggs on other hosts? We do not know. I hope someone is working on those questions as we speak and will soon surprise us with a publication.

But let me finish with a witty comment on Zimmer’s blog, by a commenter who, for this occasion, identified as “Kafka”:

“I had a dream that I was a cockroach, and that wasp Ann Coulter stuck me with her stinger, zombified my brain, led me by pulling my antenna into her nest at Fox News, and laid her Neocon eggs on me. Soon a fresh baby College Republican hatched out, burrowed into my body, and devoured me from the inside. Ann Coulter’s designs may be intelligent, but she’s one cruel god.”

That post on The Loom attracted tons of comments. Unfortunately, most of them had nothing to do with the cockroaches and wasps – Carl’s blog, naturally, attracts a lot of Creationists so much of the thread is a debate over IDC. However, Carl is happy to report that a grad student who actually worked on this wasp/cockroach pair, appeared in the thread and left a comment that, among else, answers several of the behavioral and evolutionary questions that I asked in this post.

You can watch some movies linked here and here.

BIO101 – Current Biological Diversity

In this lecture, as well as in the previous one and the next one, I tackle areas of Biology where I am really weak: origin of life, diversity of life, and taxonomy/systematics. These are also areas where there has been a lot of change recently (often not yet incorporated into textbooks), and I am unlikely to be up-to-date, so please help me bring these lectures up to standards…. This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

 

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Current Biological Diversity

In the first two parts of this lecture we tackled the Origin of Life and Biological Diversity and the mechanisms of the Evolution of Biological Diversity. Now, we’ll take a look at what those mechanisms have produced so far – the current state of diversity on our planet.

The Three Domains

The organisms living on Earth today are broadly divided into three large domains: Bacteria, Archaea and Eukarya (Protista, Plants, Fungi and Animals). Our understanding of the relationship between the three domains is undergoing big changes right now. The old divisions have been based on morphological and biochemical differences, but recent genetic data are forcing us to rethink and revise the way we think about the three Domains.

It was thought before that Bacteria arose first, that Archaea evolved from a branch off of bacterial line, while the first Eukarya (protists) evolved through the process of endosymbiosis: small bacteria and archaea finding permanent homes within the cell of larger bacteria and forming organelles. It was thought that bacteria were always simple, that Archaea are somewhat more complex, and that Eukarya are the most complex.

Neither Bacteria nor Archaea possess any organelles or subcellular compartments. The chemistry of cell walls is strikingly different between the two groups. The genes of Archaea, like Eukaryia, have introns. Until recently, it was thought that bacterial genes have no introns, however remnants of bacterial introns have been recently discovered, suggesting that Bacteria used to have introns in the past but have secondarily lost them – becoming simpler over the 3.6 billions of evolution. The enzymes involved in transcription of DNA in Archaea are much more similar to the equivalent enzymes in Eukarya than those in Bacteria.

Molecular data, as well as what we know from evolutionary theory how population size affects the strength of natural selection, a new picture has emerged. The earliest Bacteria were simple, hugging the Left Wall of Complexity. While their population sizes were still small, Bacteria evolved greater and greater complexity, leaving the left wall somewhat, evolving more complex genomes, more complex mechanisms of DNA transcription (including introns), and perhaps even some organelles. Likewise, the Archaea split off of Bacteria (or perhaps they even appeared first) and evolved much greater complexity in parallel with the Bacteria. Eukarya also split off of Bacterial tree early on and evolved its own complexity. Thus there were three groups simultaneously evolving greater and greater complexity.

Then, Bacteria and Archaea grew up in population sizes. Instead of small pockets somewhere in the ocean, now bacteria and archaea occupied every spot on Earth in huge numbers. Large population size makes natural selection very strong. Greater complexity is not fit, thus it is selected against. Thus, the originally complex bacteria and archaea became simpler over time – they turned into lean, mean evolving machines that we see today – the dominant life forms on our planet throughout its history. They lost introns, they lost organelles, and lost many complicated enzymatic pathways, each species reducing its genome and strongly specializing for one particular niche.

On the other hand, Eukarya did not grow in numbers as much. The population sizes remained small, thus the selection against complexity was relaxed – the eukaryotes were free to evolve away from the Left Wall. They increased in complexity, engulfing other microorganisms that later became mitochondria and chloroplasts.

Thus, though we, for egocentric reasons, like to think of greater complexity as being better than being simple, the Big Story of the evolution of life on Earth is that of simplification. Natural selection harshly eliminated organisms that experimented with greater complexity – the Eukarya being the exception: an evolutionary accident that happened due to their existence in small, isolated populations in which selection against complexity is relaxed.

Bacteria

Bacteria are small, single-celled organisms with no internal structures or organelles. Bacteria may have cell walls on the surface of their cell membranes, and may have evolved cilia or flagella for locomotion. The DNA is usually organized in a single circular chromosome. Some bacteria congregate into colonies or chains, while in other species each cell lives on its own.

In the laboratory, bacteria can be easily separated into two major groups by the way their cell walls get stained by a particular stain into Gram positive (purple stain) and Gram negative (red stain) bacteria. By shape, bacteria are divided into cocci (spherical cells), bacilli (rod-like shapes) and spirilli (thread-like or worm-like cells).

Bacteria are capable of sensing their environment and responding to it – i.e., they are capable of exhibiting behavior. Bacteria are also capable of communicating with each other – for instance, they can sense how many of them are present in a particular place and they can all change their behavior once the population size reaches a certain threshold – this kind of sensing is called quorum sensing.

Many bacteria are serious pathogens of plants and animals (including humans). Others are important decomposers of dead plants and animals, thus playing important roles in the ecology of the planet. Yet others are symbionts – living in mutualistic relationships with other organisms, e.g., with plants and animals.

Deinococcus radiodurans is one famous bacterium. It thrives inside nuclear reactors. Of course, our reactors are a very recent innovations, so the scientists were puzzled for a long time as to what natural environment selected these organisms to be able to survive in such a harsh environment. It turns out that dehydration (drying-out) has the same effects on the DNA as does radioactivity – fragmenting and tearing-up of pieces of the DNA molecule. Deinococcus evolved especially fast and accurate mechanisms for DNA repair. Bioengineering projects are underway to genetically engineer these bacteria in such a way that they can be used to clean up radioactive spills and digest nuclear waste.

The inside of out digestive tract provides a home for numerous microorganisms. The best way to think about out “intestinal flora” is in terms of an ecosystem. We acquire it at the moment of birth and build it up with the bacteria we get from the environment – mostly from our parents. The bacterial populations in the intestine go through stages of building an ecosystem, similarly to the secondary succession. If, due to disease or due to use of potent antibiotics, the balance of the ecosystem is disrupted, it may recover through phases akin to primary succession.

Experiments with completely internally sterile animals (mostly pigs and rabbits) demonstrated that we rely on our intestinal bacteria for some of our normal functions, e.g., digestion of some food components, including vitamins. In many ways, after millions of years of evolution, our internal bacteria have become an essential part of who we are, and there is now a push for sequencing the complete genome of our bacterial flora and to include that information in the Human Genome. The composition of the bacterial ecosystem in out guts can affect the way we respond to disease, or even if we are going to get fat or not, thus there is much recent research on individual variation of the intestinal flora between human individuals, so-called “poo print” (yes, scientists do have a sense of humor).

Archaea

Archaea may have been the first life forms on the Earth. Today, they tend to occupy niches that no other organisms can. Thus, they are found living inside the rocks miles under the surface, they are found in extremely cold and extremely hot environments, in very salty, very acidic and very alkaline environments as well. The hot water of the Old Faithful geyser in Yellowstone national park are inhabited by a species of Archaea. They are difficult to study as they die in normal conditions in the laboratory – room temperature, neutral pH etc.

Though some Archaea have been found to live inside our bodies, not a single one has, so far, been identified as a pathogen. Only very recently (i.e., last few weeks) has it been shown that one Archaean does have an effect on our health – not as a pathogen but as an enabler. It can migrate into roots of our teeth and set up colonies there. It then changes the environment in the tooth in such a way that it becomes conducive to the immigration and reproduction of a pathogenic bacterium than can then attack the tooth.

Protista

Protists are an artificial group of organisms – every eukaryote that cannot be classified as a plant, a fungus or an animal is placed in this category. Thus, the number of species of protists is very large and the diversity of shapes, sizes and types of metabolism is enormous.

Some protists are microscopic unicellular organisms, like the Silver Slipper (Paramecium), while others are multicellular and quite large (e.g, sea kelp). Some protists, e.g., cellular slime molds, have a single-celled and a multi-celled phase of their life-cycle.

Even some of the unicellular protists can be quite large – an Acetabularia (‘mermaid’s wineglass’, see picture) cell is about 5 cm long, thus perfectly visible to the human eye. Most protists reproduce regularly by asexual processes, e.g., fission or budding, utilizing sexual reproduction (e.g., conjugation, which is gene-swapping) only in times of stress. Some protists are surrounded only by a plasma membrane, while some others form shells of silica (glass) around themselves. Some protists have flagella or cilia, while some others move by pseudopodia (false legs – ameboid movement).

Traditionally, protists have been artificially subdivided into three basic groups according to their metabolism: protists capable of photosynthesis (autotrophs) are called Algae, heterotrophs are called Protozoa, while the absorbers are Fungus-like protists. According to morphology, protists have been divided into about 15 phyla, grouped into six major groups. New molecular techniques are thoroughly changing the taxonomy and systematics of Protista. One group, the Green Algae, has recently been moved out of Protista and into the Kingdom Plantae. Another group, the Choanoflaggelata, has been moved to the Kingdom Animalia as they are most closely related to sponges.

Some protists are parasites that cause human diseases. Most well-known of those are Plasmodium (malaria), various species of Trypanosoma (sleeping sickness, leischmaniasis and Chagas Disease) and Giardia (Hiker’s Diarrhea). Dinoflagellates live on the surface of the ocean and are almost as important for absorption of CO2 and production of O2 as are forests on land.

Plants

Plants are terrestrial, multicellular organisms capable of photosynthesis (though some species have secondarily moved back into the aquatic environment or lost the ability to photosynthesize). There are about 300,000 species of plants on Earth today. They are divided into two broad categories: non-vascular and vascular plants. Mosses, liverworths and some other smaller groups are non-vascular plants. All other plants are vascular, meaning that they possess systems of tubes and canals that are used to transports water and nutrients from root to stem and leaves, and from leaves back to the root. Those tubes and canals are called phloem and xylem.

Of the vascular plants, some reproduce by forming spores, while others produce seed. Seedless vascular plants that produce spores are, among others, ferns and horsetails. Seeds are produced by two large groups: Gymnosperms (e.g., conifers) and Angiosperms (flowering plants).

An important evolutionary trend in plants was a gradual reduction of the haploid portion of the life-cycle (gametophyte) and simultaneous rise to dominance of the diploid portion – the sporophyte. In mosses, for instance, almost all of the plant is haploid, except for the diploid spores developing at the very tip of the stem. In flowering plants, e.g., trees, almost all of the plant’s cells are diploid (just like in us), while the flowers contain male and female gametes (pollen and egg).

Fungi

Fungi can be unicellular (e.g., some yeasts and molds) or multicellular (e.g, mushrooms). Molecular data show that fungi are more closely related to animals than plants. Fungi are heterotrophs that obtain nutrients from the soil by secreting enzymes into the substrate and absorbing the digested materials. They cannot photosynthesize. Fungi are composed of hyphae, which are thin long filaments. A mass of hyphae is called the mycelium which can build large structures like mushrooms. Spores are the means of reproduction and are formed by sexual or asexual processes.

Fungi tend to enter into symbiotic relationships with other organisms. Some of those relationships are parasitic, as in our own fungal diseases. Other relationships are mutualistic, e.g., lychens, mycorrhizae and endophytes. Lichens are a mutualistic association between a fungus and a photosynthesizer, usually a green algae. Mycorrhizae form mutualistic associations between the fungi and plant roots (e.g., alfalfa). Endophytes are plants that have fungi living inside them in intercellular spaces and may provide protection against herbivores by producing toxins.

Animals

Animals are multicellular heterotrophs (they do not photosynthesize). They exhibit embryonic development and mostly reproduce sexually. One of the important characteristics of animals is movement. While microorganisms (bacteria, archaea and small protists) can move, large organisms (large protists, plants and fungi) cannot – they are sessile (attached to the substrate). Animals are large organisms that are capable of active movement: swimming, crawling, walking, running, jumping or flying. While some animals are also sessile, at least one phase of their life-cycle (e.g., a larva) is capable of active movement.

Some of the major transitions in the evolution of animals are evolution of tissues, evolution of symmetry (first radial, later bilateral), evolution of pseudocoelom and coelom, the difference between Protostomes and Deuterostomes, and the evolution of segmentation.

There are about 37 phyla of animals. Animals can be divided into two sub-Kingdoms: Parazoans and Eumetazoans. Parazoans are choanoflagellates and sponges. They do not have tissues – their cells are randomly organized. A sponge can be pushed through a sieve and all cells get detached from each other during the process, yet they will reconnect and form an intact sponge afterwards. Sponges move by reorganization of the whole body – cells move over each other (pulling the silicate spicules along) and can move as much as 6mm per day. All other animals are Eumetazoans – their cells are organized within proper tissues.

Parazoans also have no body symmetry. Some phyla of animals (e.g, Cnidaria) have radial symmetry – they are called Radiata. Most phyla of animals – the Bilateria – have bilateral symmetry: the left and the right side of the body are mirror images of each other. In bilaterally symmetrical animals, there is early embryonic determination not juts of up-down axis, but also of front-back axis. Bilateral symmetry gives the animal direction – it moves in one direction, the sensory organs and the mouth tend to be in front, while excretion and reproduction are relegated to the back of the animal.

Early during development, the cells of the spherical embryo (gastrula) organize into layers. Some animals (Diploblasts) have only two layers: ectoderm on the outside and endoderm on the inside. Most animals (Triploblasts) have evolved a third layer in between – the mesoderm. Ectoderm gives rise to the skin and nervous system. Endoderm gives rise to the intestine and lungs, among else. Mesoderm gives rise to muscles and many other internal organs. Usually, Radiata are Diploblasts, while Bilateria are Triploblasts.

In more primitive animals, there is no internal body cavity (e.g., flatworms). In others, a cavity forms during the development between the endoderm and mesoderm – it is called pseudocoelom (e.g., nematodes). In most animals, a proper coelom develops between two layers of mesoderm. Our abdominal and chest cavities are parts of our coelom.

In most phyla of animals, the early embryo divides by spiral cleavage. The blastopore – an opening into the cavity of the blastula- eventually becomes the mouth. These animals are called Protostomes. Protostomes are further divided into two groups: in one group animals grow by adding body mass (e.g., annelids, molluscs and flatworms), while others grow by molting (e.g., nematodes and arthoropods).

In Echinodermata and Chordata, the embryo divides by radial cleavage. The blastopore becomes the anus. These animals are Deuterostomes.

Three large phyla of animals – Annelida, Arthropoda and Chordata evolved segmentation, using Hox genes to drive the development of each segment.

You will HAVE to read the three relevant animal chapters in the textbook to learn more about the following phyla: sponges, cnidarians, annelids, molluscs, arthropods and chordates.

Phylum Chordata is the one we are most interested in for egocentric reasons – because we are chordates. The phylum consists of some invertebrate groups and the Vertebrata (all other animal phyla are also Invertebrata). The invertebrate chordates are hemichordates (acorn worms), tunicates (Urochordata – sea squirts) and cephalochordates (e.g., the lancelet – Amphioxus, see picture). The larvae of invertebrate chordates are very similar to the larvae of echinoderms, both groups are also Deuterostomes, and recent molecular data confirm close relationship between chordates and echinoderms as well.

All chordates have, at least at some point during the development, a notochord. The early chordates were aquatic animals. Hagfish and lampreys are two of the most primitive groups of vertebrates. Before the molecular analysis was performed, these two groups were clumped into a single group of Jawless Fish (Agnatha), but have since been split into two separate classes.

‘Fish’ is the lay term for several different groups of aquatic vertebrates. The most important classes are cartilagenous fish (Chondrichthyes, e.g., sharks, rays and sturgeons), lobe-finned fish (Sarcopterygii, e.g., gars) and ray-finned fish (Actinopterygii – most fish that you can think of). The latter two of those are also sometimes lumped together and called the bony fish (Teleostei). Chrossopterygii, a once-prominent group of lobe-finned fish that survives today with only one living species (Coelacanth, or Latimeria), is the group that gave rise to ancient amphibians – the first vertebrates to invade the land (check out the Tiktaalik website for more information).

Amphibians are frogs, toads, salamanders and cecilians. At least one portion of the life-cycle – reproduction and early development – is dependent on water. They have legs for locomotion and lungs for respiration on land.

Reptilia are a large and diverse class of vertebrates. They include lizards, snakes, tuataras, turtles, tortoises and crocodilians. They have scaly skins that allows them to survive in arid environments. They have evolved an amniotic egg – an egg that contains nutrien-rich yolk and is contained within a leathery shell. Thus, reproduction and development are not dependent on water. Many reptiles live in deserts.

A now-extinct group of ancient reptiles (therapsyds) gave rise to mammals (class Mammalia) about 220 million years ago. The early mammals were quite large carnivores. However, during the 150 million year reign of the Dinosaurs (another extinct group of reptiles) mammals were constrained to a very small niche – that of nocturnal burrowing insectivores. Only after the demise of Dinosaurs (65 million years ago) could mammals embark on a fast evolutionary radiation that produced groups we know now.

Birds and mammals are endotherms – they can control (and keep constant) their body temperature by producing the heat in organs like muscles and liver. This is a metabolically expensive strategy that requires these animals to eat very frequently, but gives them speed and stamina and allows these animals to live in every part of the Earth, incuding polar regions. Other vertebrate classes are ectotherms – they gain their heat from the environment and, if they are cold, they are slow and sluggish.

As it is very difficult for large bodies to lose heat, large reptiles (like dinosaurs), once heated, can retain their body temperature for long periods of time – they are effectively warm-blooded. Some reptiles, notably pythons and iguanas, are capable of producing some of the heat internally. While they cannot keep a constant body temperature, they are capable of some degree of thermoregulation (e.g., becoming somewhat warmer than the external environment). By shivering their muscles, pythons raise their body temperature above ambient and use this heat to incubate their eggs.

There are about 4500 species of mammals, organized into 19 orders. The defining characteristics of mammals are milk ­producing glands and hair.

Monotremes (platypus and echidna) are egg-laying mammals. Their mammary glands are not completely evolved yet – the young lick the milk of off mothers hair.

Marsupials are the pouched mammals (e.g., kangaroo, koala, opossum). The immature newborn offspring crawls up into the pouch and lives inside it until they are large enough to fend for themselves.

Placental mammals (the remaining 17 orders) have a placenta that nourishes their embryos during development. The new molecular data, coupled with a number of exciting newly-discovered fossils, are changing our understanding of genealogical relationships between different orders of mammals, including our new knowledge about the evolution of whales, the relationship between elephants and hyraxes, between Carnivores and Pinnipedieans (seals, etc.) and between rodents and rabbits.

The most recent vertebrate class – the birds (Aves) – evolved out of a branch of Dinosaurs. There are 28 orders of bird in 166 families. Two primary characteristics distinguish birds from reptiles: feathers and flight skeleton. Their feathers are modified reptile scales. Feathers are obviously important for flight, but also insulate as birds are endotherms.

Previously in this series:

BIO101 – Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype
BIO101 – From Genes To Species: A Primer on Evolution
BIO101 – What Creatures Do: Animal Behavior
BIO101 – Organisms In Time and Space: Ecology
BIO101 – Origin of Biological Diversity
BIO101 – Evolution of Biological Diversity

BIO101 – Evolution of Biological Diversity

In this lecture, as well as in the previous one and the next one, I tackle areas of Biology where I am really weak: origin of life, diversity of life, and taxonomy/systematics. These are also areas where there has been a lot of change recently (often not yet incorporated into textbooks), and I am unlikely to be up-to-date, so please help me bring these lectures up to standards…. This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

In the previous segment of the lecture, we looked at the Origin of Life and the beginnings of the evolution of biological diversity. Now we move to explanations of the mechanisms by which diversity arises.

Although traits can be inherited by non-DNA ways, and DNA sequence does not necessarily translate directly onto the traits, in the long term the differences between species tend to be recorded in the genome. Thus, differences between genomes of different species are most important differences between them. How do differences between genomes arise? There are six major (and some minor) ways this happens:

Mutations are small changes in the sequences of DNA. Some of the changes are just substitutions of one nucleotide with another, others are deletions, insertions and duplications of single nucleotides or small strings of nucleotides within a gene, or within a non-coding regulatory sequence. Such small changes may alter the function of the gene-product (protein) which may translate into changes in traits which may be selected for by natural or sexual selection.

Gene duplication occurs quite often due to errors in DNA replication during cell division, or due to errors in ‘crossing-over’ phase of meiosis. Instead of a single copy of a gene, the offspring have two copies of that same gene. As long as one copy remains unaltered and functions properly, the other gene is free to mutate (i.e., there will stabilizing selection on the first copy, and no selection for the preservation of the sequence of the second copy). The second gene may transiently become non-functional, but as it keep mutating it may begin coding for a completely novel protein which will start interacting with other molecules in the cell. If this new interaction confers increased fitness on the organism, this new gene sequence will become selected for and fine-tuned by natural (or sexual) selection for its new function.

Chromosome duplication may also occur due to errors in DNA replication during cell division. Instead of just one gene being duplicated, a large number of genes now exist in two copies, each pair of copies consisting of one copy that is preserved by stabilizing selection and another copy that is free to mutate and thus potentially evolve novel traits.

Genome duplication has occurred many times, especially in plants. The whole genome doubles, i.e., all of the chromosomes are duplicated. The resulting state is called polyploidy. This provides a very large amount of genetic material for natural selection to tinker with and, over time, produce novel traits.

Rearrangement of segments of the DNA along the same chromosome, or between chromosomes, places different genes that were once far from each other into closer proximity. Thus, genes that were previously quite independent from each other may now be expressed together or may start influencing each others expression. Thus, the genes become linked together (or unlinked from each other), restructuring the batteries of genes that work together in a common function. This may free some genes to evolve independently, while tying some genes together and thus constraining the direction in which development of traits may evolve.

Lateral transfer (sometimes called ‘horizontal transfer’) is an exchange of DNA sequences between individuals of the same species or of different species. While vertical transfer moves genes from parents to offspring, lateral transfer moves genes between unrelated individuals. Such transfer is very common in microorganisms. Some species of Bacteria, Archaea and Protista routinely engage in gene swapping, which results in increase of genetic diversity of the species and thus provides raw material for evolution to build new traits. Gene swapping between organisms of different species may transfer a complete function from one species to another. Sometimes viruses act as carriers of genes from one species to another. For instance, a virus may take a piece of a bacterial genome and later insert it into a genome of a plant or a mammal. Some key genes involved in the development of the placenta originated as bacterial genes inserted into early mammalian genomes via viruses.

One important thing to bear in mind is that evolution has to ensure the survival of the individual at all stages of its life-cycle, not just the adult. Thus, evolution of new traits can occur only if it does not disrupt the viability of eggs, larvae, immature adults and mature adults.

Another important thing to keep in mind is that traits arise through embryonic and post-embryonic development. Thus, evolution of traits is really evolution of development. Evolution of genomes, thus, is not evolution of random grab-bags of many genes, but evolution of complexes of genes involved in development of particular traits.

A product of a gene is a protein. A protein that is capable of binding to DNA and thus regulating the expression of other genes is called a transcription factor. When bound to a gene, a transcription factor may induce its expression, block its expression, or increase or decrease the rate of its expression. The patterns of gene expression are key to embryonic development and cell differentiation, so it is not surprising that transcription factors play a large role in evolution of new traits via development.

A novel pattern of gene expression may arise in two ways. First, by mutation of a transcription factor (so-called trans-factors), it changes which genes it affects and the way it affects them. Second, by mutations in regulatory regions (so-called cis-factors) of the target genes, the transcription factors may or may not bind to them, or a different transcription factor may bind to them, or the effect of the binding on transcription of the gene may change.

Most important genes in evolution of development are transcription factors. Often, they work in batteries (or complexes or toolkits), where one gene induces transcription of the second gene which in turn induces transcription of the third gene, and so on. Such batteries tend to be strongly preserved in many species of living organisms, though the genes that act as final targets of action of such complexes differ between species. Such complexes may determine what is up and what is down in an early embryo, or what is forward and what is bakward in an embryo. Such complexes are used over and over in evolution to produce protruding structures, like limbs. Another such complex has been used in 40 different groups of animals for the construction of 40 quite different types of eyes.

Possibly the most important such complex in animals is the complex of Hox genes that regulates segmentation. Most animals are segmented. While this is obvious in earthworms where all segments look alike, in many other animals segments are formed in the early embryo and each segment then develops unique structures on it. Thus, an insect will develop jaws and antennae on its head segment, wings and legs on its thoracic segment, and reproductive structures and stings on its abdominal segment. You will need to carefully read the handout “A Brief Overview of Hox Genes” and be able to define Homeotic genes, Homeobox (DNA sequence), Homeodomain (protein structure) and Hox genes. Interestingly, non-segmented Cnidarians (corals and jellyfish) do not have true Hox genes, though they do have scatterings of Hox-like genes, which may be evolutionary precursors of true Hox genes.

Thus, evolution of diversity can be thought of in terms of changes in the way developmental toolkits are applied in each species. The same toolkits are used over and over for development of similar traits. The sequences of the genes within the toolkits will vary somewhat between species, and the sequences of genes that are final targets of action of toolkits will vary much more.

Thus, with quite a limited number of genetic toolkits, nature can develop a myriad different forms, from cabbages and sponges to honeybees and humans. This also explains why we do not need more than 30,000 genes to develop a human, as well as why our genome is about 99% identical to the chimpanzee genome. It is not the sequence of genes, but the combinatorics of the way the genes are turned on and off during the development that results in the final phenotype.

The common theme, then, is that evolution keeps tinkering with the same genetic toolkits over and over again. It is not necessary to evolve thousands of completely new genes in order to have a new species spring up out of its ancestral species. A little tweak in developmental patterns of gene expression is all that is needed. The same genes may be expressed at a different place in the embryo in two different species (heterotopy), or may be expressed at a different time during development (heterochrony), or may result in expression of other final-target genes (heterotypy). Such changes account for most of the evolution of diversity of life on Earth.

Of course, such changes take a long time. It took about 3.6 billion years for life to evolve from the first primitive bacteria-like cells to the current diversity of millions of species of Bacteria, Archaea, Protista, Fungi, Plants and Animals. Our brains have never before needed to be able to comprehend such vastness of time. We do quite well with durations of seconds, minutes, hours and days. We are pretty good at mentally picturing the duration of weeks, months and years. A decade is probably the longest duration of time that our brains can correctly imagine. Already our perception of a century is distorted. Perception of a thousand years is impossible for human brains. Now try to imagine how long 10,000 years is? Any luck? Now try 100,000. How about 1.000,000 years? Add another zero and try comprehending 10.000,000 years. Multiply by ten again and try 100.000,000 years. Now try 1,000.000,000 years. Now try four times more – 4 billion years.

It is not surprising that some people, unable to comprehend 4 billion years, just plainly refuse to acknowledge that this amount of time actually passed and stick to a shorter, emotionally more pleasing yet incorrect number of about 6,000 years for the age of the Universe. Such people, of course, cannot believe that evolution actually happened, although mountains of evidence show us not just that it happened, but exactly how it happened. You can see exactly what happened when if you take your time and do this animation. You’ll notice how the whole of human history is too short to be visible on a line representing billions of years. Given such enormous amount of time, the evolution of amazing diversity of life is not surprising. Actually, if such diversity did not arise – that would be a surprise.

Watch Animation:

Evolution

Handouts:

A Brief Overview of Hox Genes
Bat Development
How To Make A Bat

Additional Readings:

Jellyfish Lack True Hox Genes

Previously in this series:

BIO101 – Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype
BIO101 – From Genes To Species: A Primer on Evolution
BIO101 – What Creatures Do: Animal Behavior
BIO101 – Organisms In Time and Space: Ecology
BIO101 – Origin of Biological Diversity

BIO101 – Origin of Biological Diversity

This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

Adaptation vs. Diversity

Biology is concerned with answering two Big Questions: how to explain the adaptation of organisms to their environments and how to explain the diversity of life on Earth.

Much of the course content so far engaged the question of the origin and evolution of adaptation, and much of the remainder of the course will also look at particular adaptations of humans and other vertebrates. This is the only lecture specifically targeting the question of diversity.

The way this material is usually taught is to go over long lists of organisms and tabulate their characters, how the members of one group are similar to each other and different from members of other groups. We, in our course, will try a different approach, i.e., not just describing, but also explaining diversity – how it comes about.

If you think about it, knowing what we learned so far about the way evolution works, the origin of adaptation and the origin of diversity are deeply intertwined: as local populations evolve adaptations to their current local environments, they become more and more different from each other until the species splits into two or more new species. Thus, evolution of adaptations to local conditions leads to proliferation of new species, thus to the increase in overall diversity of life on the planet.

Origin of Life

One can postulate four ways the life on Earth came about: a) it was created – poof! – out of nothing by an intelligent being, e.g., God; b) it was created – poof! – out of nothing by an intelligent being, e.g., space aliens, either on Earth or elsewhere, then brought to Earth; c) it spontaneously arose elsewhere in the Universe and was brought to Earth by comets and meteors; and d) it spontaneously arose out of chemical reactions in the ancient seas in the presence of the ancient atmosphere.

Science is incapable of addressing the first notion – being untestable and unfalsifiable (impossible to prove that it is wrong), it is properly outside of the realm of science and within the domain of religion.

The first three notions also just move the goalposts one step further – how did life (including God and/or Aliens) arise elsewhere in the Universe? Thus, scientists focus only on the one remaining testable hypothesis – the one about spontaneous and gradual generation of life out of non-life, a process called abiogenesis. The scientific study of abiogenesis cannot say and does not attempt to say, anything about existence of God or Aliens. It only attempts to figure out how life could have arisen on its own, sometime between 3 and 4 billion years ago.

All of life on Earth descends from a single common ancestor. It is quite possible that life initially arose multiple times, but as soon as one life form became established and competitive enough, all the other instances of spontaneous generation of life were out-competed and did not leave progeny.

It is difficult to study the origin of life as molecules do not leave fossils. They do leave chemical traces, though, so we know a lot about the chemistry of the ancient oceans, soil and atmosphere. Thus, we know under what conditions and what available materials (and energy) life first arose. By replicating such conditions in the laboratory, we can study the details of how life might have evolved out of non-life.

The study of the origin of life is a lively and exciting area of biology, perhaps because so little has yet been settled with great certainty. There are a number of competing hypotheses promoted by various research groups. Those hypotheses can be classified into groups: RNA First, Protein First, RNA-Protein First and Bubbles First.

RNA is a molecule that can be replicated and thus can serve as the original hereditary material (DNA is too large and complex even for some of today’s viruses, let alone for the first simple organisms). RNA is also capable of catalytic activity – promoting and speeding up reactions between other molecules, as well as replicating itself. Thus, RNA is the best candidate for the first molecule of life. Still, it is not capable of everything that life needs, so a few simple polypeptides (and those are really easy to synthesize in a flask mimicking the original Earth conditions) were probably involved from the very beginning. For those reactions to occur, they had to be separated from the remaining ocean – thus some kind of “cell membrane”, like a soap bubble, was also necessary for the origin and early evolution of life.

Those early “cells” competed against each other. Those that, through chemical evolution, managed to become good enough at remaining stable for a decent amount of time, capable of acquiring the energy from the environment, and capable of dividing into two “daughter cells” out-competed the others – chemical evolution turned into biological evolution. As they changed through trial and error, some cells gradually got better at “living” and out-competed all others. One best competitor of the early living world is the common ancestor of all of the subsequent life on Earth, including us.

Directionality of Evolution

There are two common misconceptions about evolution. First is the idea that evolution tends towards perfection. But, always remember that evolution favors individuals who are slightly better optimized to current local conditions than other individuals of the same species, i.e., what wins is the relative fitness, not absolute fitness (i.e., perfection). In other words, you have to be capable of surviving and reproducing in your current environment and be just a tad little bit better at it than your conspecifics – there is no need to be perfectly adapted.

The second common misconception about evolution is that it has a tendency to generate greater complexity. Originally, right after the initial origin of life on Earth, evolution did produce greater complexity, but only because there was no way to become any more simple than the first organisms already were. There is a “left wall” of complexity in the living world, i.e. there is a minimum complexity that is necessary for something to be deemed alive.

Thus, initially, the only direction evolution could take was away from the left wall (red dot), i.e., becoming more complex. But once reasonably complex organisms evolved, they were not snuggled against the left wall any more (yellow dot). Adaptation to current local conditions can equally promote simplification as it does complexification of the organism in question. In other words, as populations evolve, the members of the populations are equally likely to become simpler as they are to become more complex.

Actually, as we know from the world of man-made machines, there is such a thing as being too complex (blue dot). Over-complicated machines break down much more easily and are more difficult to maintain and repair. Likewise, organisms of great complexity are often not as fit as their simpler relatives – their genomes are so large that the error rate is greater and cell division is more difficult. Cells can “go wild” and turn into cancer. Also, with so many interacting parts, it is more difficult for complicated organisms to evolve new adaptations as the development of the whole complex system has to change and adapt to such changes.

Thus, simplification is as often seen in evolution as is acquisition of greater complexity. Just think of parasites – they are all simplified versions of their free-living relatives – no need for eyes, other sensory organs or means of locomotion if one spends one’s life attached to the lining of the host’s intestine, sucking in nutrients and growing billions of eggs.

Measuring Diversity – Taxonomy and Systematics

People have always tried to classify living beings around them, by grouping them according to some man-made criteria, usually by the way they look, where they live, and how useful they may be to us. Only for the past 150 years we have understood that all organisms on our planet are genealogically related to each other, so we started classifying them according to the degree of relatedness – drawing family trees of Life.

Initially, classification was done according to anatomy and embryology of organisms. Such methods brought about the division of Life on Earth into six great Kingdoms: Bacteria, Archaea, Protista, Plants, Fungi and Animals. The first two are Prokaryotes (cell has no nucleus), the latter four are Eukaryotes (cells have a nucleus).

The Kingdoms were, like Russian dolls, further subdivided into nested hierarchies: each Kingdom was composed of a number of Phyla (Phylum = type). Each Phylum consists of Classes, those are made of Orders that are further subdivided into Families. Each family consists of Genera and each Genus is composed of the most closely related Species.

The proper name of each living organism on Earth is its binomial Latin name – capitalized name of the Genus and lower-case name of the species, both italicized, e.g., Homo sapiens, Canis familiaris, Equus caballus, Bos taurus (human, dog, horse and cow, respectively).

Lately, modern molecular genetic techniques have been applied to testing relationships between species, resulting in many changes in classification at lower levels of systematics (e.g,. species, genus, family, etc).

The knowledge gained from this approach also resulted in some big changes in the way we classify living organisms. Instead of six Kingdoms, we now divide life on Earth into three Domains: Bacteria, Archaea and Eukarya.

We are now aware that endosymbiosis (intercellular parasites, originally small bacterial cells entering and living inside larger bacterial cells) gave rise to organelles, like mitochondria and chloroplasts. We are now aware how much lateral (or horizontal) transfer of genetic material is going on between species, i.e., the branching tree of life has many traversing connections between branches as well.

Cladistics is a relatively new method of classifying organisms, using multiple (often many) different genetic, morphological and other traits and building “trees” by calculating (using computer software) the probabilities of each two of the species being related to each other. Thus, “most likely” trees are plotted as cladograms which can further be tested and refined.

Previously in this series:

BIO101 – Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype
BIO101 – From Genes To Species: A Primer on Evolution
BIO101 – What Creatures Do: Animal Behavior
BIO101 – Organisms In Time and Space: Ecology

Cicadas, or how I Am Such A Scientist, or a demonstration of good editing

Originally published on May 16th, 2011 at my old blog.

Charles Q. Choi runs a bi-weekly series on the Guest Blog over at Scientific American – Too Hard for Science? In these posts, he asks scientists about experiments that cannot be or should not be done, for a variety of reasons, though it would be fun and informative it such experiments could get done.

For one of his posts, he interviewed me. What I came up with, inspired by the emergence of periodic cicadas in my neighborhood, was a traditional circadian experiment applied to a much longer cycle of 13 or 17 years.

Fortunately for me, Charles is a good editor. He took my long rant and turned it into a really nice blog post. Read his elegant version here – Too Hard for Science? Bora Zivkovic–Centuries to Solve the Secrets of Cicadas.

Now compare that to the original text I sent him, posted right here:

The scientist: Bora Zivkovic, Blog Editor at Scientific American and a chronobiologist.

The idea: Everything in living organisms cycles. Some processes repeat in miliseconds, others in seconds, minutes or hours, yet others in days, months or years. Biological cycles that are most studied and best understood by science are those that repeat approximately once a day – circadian rhythms.

One of the reasons why daily rhythms are best understood is that pioneers of the field came up with a metaphor of the ‘biological clock‘ which, in turn, prompted them to adapt oscillator theory (the stuff you learned in school about the pendulum) from physics to biology.

And while the clock metaphor sometimes breaks down, it has been a surprisingly useful and powerful idea in this line of research. Circadian researchers came up with all sorts of experimental protocols to study how daily rhythms get entrained (synchronized) to the environmental cycles (usually light-dark cycles of day and night), and how organisms use their internal clocks to measure other relevant environmental parameters, especially the changes in daylength (photoperiod) – information they use to precisely measure the time of year and thus migrate, molt or mate during an appropriate season.

These kinds of experiments – for example building Phase-Response Curves to a variety of environmental cues, or a variety of tests for photoperiodism (night-break protocol, skeleton photoperiods, resonance cycles, T-cycles, Nanda-Hamner protocol etc.) – take a long time to perform.

Each data point requires several weeks: measuring period and phase of the oscillation before and after the pulse (or a series of pulses) of an environmental cue in order to see how application of that cue at a particular phase of the cycle affects the biological rhythm (or the outcome of measuring daylength, e.g., reproductive response). It requires many data points, gathered from many individual organisms.

And all along the organisms need to be kept in constant conditions: not even the slightest fluctuations in light (usually constant darkness), temperature, air pressure, etc. are allowed.

It is not surprising that these kinds of experiments, though sometimes applied to shorter cycles (e.g., miliseconds-long brain cycles), are rarely applied to biological rhythms that are longer than a day, e.g., rhythms that evolved as adaptations to tidal, lunar and annual environmental cycles. It would take longer to do than a usual, five-year period of a grant, and some experiments may last an entire researcher’s career. Which is one of the reasons we know so little about these biological rhythms.

~~~~~~

Living out in the country, in the South, just outside Chapel Hill, NC, every day I open the door I hear the deafening and ominous-sounding noise (often described as “horror movie soundtrack) coming from the woods surrounding the neighborhood. The cicadas have emerged! The 13-year periodic cicadas, that is. Brood XIX.

I was not paying attention ahead of time, so I did not know they were slated to appear this year in my neck of the woods. One morning last week, I saw a cicada on the back porch and noticed red eyes! A rule of thumb that is easy to remember: green eyes = annual cicadas, red eyes = periodic cicadas. I got excited! I was waiting for this all my life!

Fortunately, once they emerge, cicadas are out for a few weeks, so my busy travel schedule did not prevent me from going to find them (just follow the sound) to take a few pictures and short videos.

There are three species of periodic cicadas that emerge every 17 years – Magicicada septendecim, Magicicada cassini and Magicicada septendecula. Each of these species has a ‘sister species’ that emerges every 13 years: M.tredecim, M. tredecassini and M.tredecula. A newer species split produced another 13-year species: Magicicada neotredecim. The species differ in morphology and color, while the 13 and 17-year pairs of sister species are essentially indistinguishable from each other. M.tredecim and M.neotredecim, since they appear at the same time and place, differ in the pitch of their songs: M.neotredecim sings a higher tone.

So, how do they count to 13 or 17?

While under ground, they undergo metamorphosis four times and thus go through five larval instars. The 13 and 17-year cicadas only differ in the duration of the fifth instar. They emerge simultaneously, live as adults for a few weeks, climb up the trees, sing, mate, lay eggs and die.

When the eggs hatch, the newly emerged larvae fall from the trees to the ground, dig themselves deeper down, latch onto the tree roots to feed on the sap, and wait another 13 or 17 years to emerge again.

There are a number of hypotheses (and speculations) why periodic cicadas emerge every 13 or 17 years, including some that home in on the fact that these two numbers are prime numbers (pdf).

Perhaps that is a way to fool predators which cannot evolve the same periodicity (but predators are there anyway, and will gladly gorge on these defenseless insects when they appear, whenever that is, even though it may not be so good for them). Perhaps this is a speciation mechanism, lowering the risk of hybridization between recently split sister species?

Or perhaps that is all just crude adaptationist thinking and the strangeness of the prime-number cycles is in the eye of the beholder – the humans! After all, if an insect shows up every year, it is not very exciting. Numerous species of annual cicadas do that every year and it seems to be a perfectly adaptive strategy for them. But if an insect, especially one that is so large, noisy and numerous, shows up very rarely, this is an event that will get your attention.

Perhaps our fascination with them is due to their geographic distribution. Annual cicadas may also have very long developmental times, but all of their broods are in one place, thus the insects show up every year. In periodic cicadas, different broods appear in different parts of the country, which makes their appearance rare and unusual in each geographic spot.

In any case, I am more interested in the precision of their timing than in potential adaptive explanations for it. How do they get to be so exact? Is this just a by-product of their developmental biology? Is 13 or 17 years just a simple addition of the duration of five larval stages?

Or should we consider this cycle to be an output of a “clock” (or “calendar”) of sorts? Or perhaps a result of interactions between two or more biological timepieces, similarly to photoperiodism? In which case, we should use the experimental protocols from circadian research and apply them to cicada cycles.

Finally, it is possible that a ling developmental cycle is driven by one timing mechanism, but the synchronization of emergence in the last year is driven by another, perhaps some kind of clock that may be sensitive to sound made by other insects of the same species as they start digging their way up to the surface.
The problem: In order to apply the standard experiments (like construction of a Phase-Response Curve, or T-cycles), we need to bring the cicadas into the lab. And that is really difficult to do. Husbandry has been a big problem for research on these insect, which is why almost all of it was done out in the field.

When kept in the lab, the only way to feed them is to provide them with the trees so they can drink the sap from the roots. This makes it impossible to keep them in constant conditions – trees require light and will have their own rhythms that the cicadas can potentially pick up, as timing cues, from the sap. So, the first thing we need to do is figure out a way to feed them artificially, without reliance on living trees for food.

Also, we do not know which environmental cues are relevant. Is it light cycle? Photoperiod? Or something cycling in the tree-sap? Or temperature cycles? What are the roles of developmental hormones like Juvenile Hormone or Ecdysone? We would have to test all of them simultaneously, hoping that at least one of them turns out to be the correct one.

Second, more obvious problem, is time. These experiments would last hundreds of years, perhaps thousands! Some experiments rely on outcomes of previous experiments for the proper design. Who would do them? What funding agency would finance them? Why would anyone start such experiments while knowing full well that the results would not be known within one’s lifetime? Isn’t this too tantalizing for a scientist’s curiosity?

The solution? One obvious solution is to figure out ways to get to the same answers in shorter time-frames. Perhaps by sequencing the genome and figuring out what each gene does (perhaps by looking at equivalents in other species, like fruitflies, or inserting them into Drosophila and observing their effects), hoping to find out the way timing is regulated. This will probably not answer all our questions, but may be good enough.

Another way is to set aside space and funding for such experiments and place them into an unusual administrative framework – a longitudinal study guided by an organization, not a single researcher getting a grant to do this in his or her lab. This way the work will probably get done, and the papers will get published somewhere around 2835 A.D.

~~~~

See? How long and complex my text is? Now go back to the post by Charles to see again how nicely he edited the story.

Diversity of insect circadian clocks – the story of the Monarch butterfly

As the Monarch butterflies are passing through New York right now, I thought this would be a good time to republish my old January 2006 post about this butterfly (see also 2008 version):

There are pros and cons to the prevalent use of just a dozen or so species as standard laboratory models. On one hand, when a large chunk of the scientific community focuses its energies on a single animal, techniques get standardized, suppliers produce affordable equipment and reagents, experiments are more likely to get replicated by other labs, it is much easier to get funding, and the result is speedy increase in knowledge.

On the other hand, there are drawbacks. One is the narrow focus which can breed arrogance. The worst offenders are people who work with rats. They rarely put the word “rat” in the title of the paper, and often it is not even found in the abstract, introduction and discussion of the paper. One has to dig through the materials and methods to find out, although if you know about this little secret, the very fact that the species is not noted in the title is a dead giveaway that it is a paper about rats. Some of the papers dealing with humans also make the same mistake of not pointing out the species in the title.

One of the most important animal laboratory models for the study of genetics and molecular biology is the wine-fly Drosophila melanogaster. For a century now, almost all advances in knowledge in these areas came from fly research first, then this knowledge got applied to other species, e.g., mice and humans.

Last month (December 2005), a paper came out that highlights both the pros and the cons of the “model” approach. On one hand, all the techniques used in the work were developed by fruitfly researchers and are now standard methods, easily replicable between labs.

On the other hand, it shows how important it is to sometimes move away from the models and take a reality check: is the mechanism described in the model animal generalizable to other animals or is it idiosyncratic to the model. The papers dealing with models, including wine-flies (and of course rats!), often make the implicit claim for generalizibility (helps funding!) without data to support this claim.

The model of the molecular mechanism of the circadian clock has been initially developed in Drosophila melanogaster and massive research is still going on in this animal. It is regarded as a reference model in a way – models developed later in mice, bread-mold, Arabidopsis plant, Synechococcus bacterium, etc, are always compared to the fruitfly model to look for similarities and differences. In a sense, it is the ‘deafult’ model in chronobiology.

This paper took a look at a non-model animal and found out that the fruitfly mechanism does not appear to be even typical of other insects. Steven Reppert and colleages at the University of Massachusets Medical School are studying circadian system in Monarch butterflies (mainly in order to better understand migratory orientation).

In this paper they discover that the Monarch, unlike the fruitfly, has two copies of a clock gene called Cryptochrome (cry). One copy (cry1) is very similar to that of Drosophila. The other copy (cry2), however, is much more similar to the mouse version of the gene.

In the brain pacemakers of fruitflies, cry is not the core component of the clock but is a blue-light photoreceptor. In the peripheral tissues, the same gene may be a component of the clock (it represses expression of some other clock genes).

In mammals, cry is not directly photosensitive, but is a core clock gene and a strong repressor of expression of other clock genes.

In Monarchs, as they show in this paper, cry1 is responsive to light, just like the cry of fruitflies. The cry2, though, does not respond to light, but represses expression of other genes, just like the mouse cry.

The best thing about this paper, though, is that the authors then went on and looked into genebanks of several other insect species and, lo and behold, discovered cry2 in a few more insects, including moths, honeybees, mosquitoes and flour beetles. Actually, the honeybees and flour beetles appear to have ONLY the mammalian-like version of the gene.

They also plotted the phylogeny of the cry gene, showing the genealogical relationship between the fruitfly-like and mouse-like versions of cry, both versions presumably resulting from a gene duplication some time in the past (the apparent precursor, bacterial photolyase, appears as only one copy in E.coli and its function is in DNA repair).

The PERIOD protein does not enter the nucleus in the Chinese silkmoth and the Monarch butterfly. Thus, at least in these two insects, the molecular mechanism of the circadian clock must be different from that of the fruitfly. Presence of the mammalian-like version of the cry gene, a potent gene repressor, suggests that it may be fulfilling the function of Per in these species. Thus, there appears to be more than one way to run a clock in an insect and the fruitfly mechanism is not as ‘standard’ at previously thought.

And working with Monarch butterflies must be great fun!

Reference:

Haisun Zhu,1 Quan Yuan,1 Oren Froy, Amy Casselman, and Steven M. Reppert, 2005, The two CRYs of the butterfly.Current Biology, Vol 15, R953-R954, 6 December 2005.

 

BIO101 – Organisms In Time and Space: Ecology

This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

Ecology

 

Ecology is the study of relationships of organisms with one another and their environment. Organisms are organized in populations, communities, ecosystems, biomes and the biosphere.

A population of organisms is a sum of all individuals of a single species living in one area at one time.

Individuals in a population can occupy space in three basic patterns: clumped spacing, random spacing and uniform spacing.

Metapopulations are collections of populations of the same species spread over a greater geographic area. There is some migration (ths gene-flow) between populations. Larger populations are sources and smaller populations are sinks of individuals within a metapopulation.

Population size is determined by four general factors: natality, mortality, immigration and emigration.

Natality depends on a number of factors: the proportion of the population that are at a reproductive age (as opposed to pre-reproductive and post-reproductive), proportion of the reproductively mature individuals that get to reproduce, sex-ratio of the reproductives, the mating system, the fertility of individuals (sometimes affected by parasites), the fecundity (number of offspring per female), the maturation rate (the amount of time needed for an individual to attaint sexual maturity), and longevity (amount of time an individual can live after reproducing).

Mortality is affected by bad weather, predation, parasitism and infectious diseases. It depends on the mortality of pre-reproductive stages (from eggs and embryos, through larva and juveniles), mortality of reproductive stages, and mortality of post-reproductive stages (often from disease or aging).

A population can, theoretically, grow exponentially indefinitely. However, in the real world, the growth is limited by the amount of space, food (energy) and predators. Thus, the population size often plateaus at an optimal number – the carrying capacity of that population.

Some organisms produce a large number of progeny, most of which do not make it to maturity. This is r-strategy. The population size of such species often fluctuates in boom-and-bust patterns.

Other organisms produce a small number of progeny and make a heavy investment into parenting and protecting each offspring, This is K-strategy. The population size of such species grows more slowly and tends to stabilize around the carrying capacity.

All populations show small year-to-year fluctuations of population sizes around the optimum number. Some species, however, exhibit regular oscillations in population sizes. Such oscillations often involve populations of two different species, usually a predator and its prey, the most famous example being that of the snowshoe hare and the lynx.

Correct prediction of future changes in a population size is essential for the assessment of the populations viability and for its protection.

A biological community is a collection of all individuals of all species in a particular area. Those species interact with each other in various ways, and have evolved adaptations to life in each others’ presence.

Niche is a term that describes a life-role, or job-description, or one species’ position in the community. An example may be a large herbivore, a nocturnal burrowing seed-eater, a seasonal fruit-eater, etc.

Within one community only one species can occupy any particular niche. If two species share some of their niche, they are in competition with each other. If two species occupy an identical niche, they cannot coexist – one of the species will be forced to move out or go extinct.

If two species compete for the same resource (food, territory, etc.), one will utilize the resource better than the other. Competitive exclusion is a process in which one species drives another species out of the community.

Complete exclusion is not inevitable. The competition between two species can be reduced by natural selection, i.e., one of the species will be forced to assume a slightly different niche. For instant, two species can geographically partition the territory, e.g., one living at higher altitude than the other on the same mountain-side. Two species can also temporally partition the niches, for instance one remaining active at night and the other becoming active during the day.

Predation is one of the most important interaction between species in a community. Predation often causes evolutionary arms-races between predators and prey. For instance, by killing the slowest zebras, lions select for greater speed in zebras. Greater speed in zebras selects for greater speed in lions.

The most interesting examples of evolutionary arms-races between pairs of enemies are those in which the prey is dangerous to the predator, often by being toxic or venomous. For example, garter snakes and tiger salamanders on the West coast are involved in one such arms-race. Prey – the salamander – secrete tetrodotoxin from its skin. This toxin paralyzes the snake. Locally, some snakes have evolved an ability to tolerate the toxin, but the side-effect of such evolution is that these snakes are slow and sluggish – themselves more vulnerable to predation by birds.

Ground squirrels (prey) in the Western deserts have evolved immunity to rattlesnake venom, so the rattlesnakes (predators) are becoming more venomous. Similarly, and in the same area, desert mice have evolved immunity to the toxin of their prey – the scorpions, resulting in increasing toxicity of the scorpion venom in that region (but not in areas where these two species do not overlap). A Death’s-head sphynx moth steals honey from beehives and has evolved partial immunity to honey-bee venom.

Many plants have evolved thorns or toxic chemicals to ward off their enemies – the herbivores. Monarch butterflies are capable of feeding on milkweed despite this plant’s toxic content. Moreover, the Monarchs store the noxious chemical they extracted from milkweed and that chemical makes the butterflies distasteful to their own predators.

The shape and color of the prey often evolves to protect from predation. Warning coloration, usually in very bright colors, informs the predators that the prey is dangerous. Aposomatic coloration is one commonly found kind of warning coloration – the black and yellow stripes on the bodies of many bees and wasps are almost a universal code for dangerous venomous stings.

Cryptic coloration, or camouflage, on the other hand, allows an animal to blend in with its surroundings. Many insect look like twigs, leaves or flowers, effectively hiding them from the eyes of predators. Some animals have evolved behavioral color-change, e.g., chameleons, some species of cuttlefish and the flounder.

Batesian mimicry is a phenomenon in which non-toxic species evolve to resemble a toxic species. Thus, some butterflies look very similar to Monarch butterflies and some defenseless flies and ants have aposomatic coloration.

Mullerian mimicry is a phenomenon in which two or more dangerous species evolve to look alike. This is “safety in numbers” strategy as a predator who tastes and spits out one of them, will learn to avoid all of them in the future.

Co-evolution does not occur only between enemies. It can also occur between species that positively affect each other. The best example is co-evolution of flowers and insect pollinators.

Symbiosis is a relationship between organisms that are not direct enemies (e.g,. predator and prey) to each other. Commensalism, mutualism and parasitism are forms of symbiosis.

In commensalism, one partner benefits, while the other one is not affected at all. For instance, birds building nests in a tree do not in any way affect the fitness of the tree.

Mutualism benefits both partners. The best known examples are lichens, mycorrhizae, and legumes. Birds that clean the skin or teeth of crocodiles, hippos or rhinos are protected by their hosts.

Parasitism is detrimental to one of the partners. Parasites that are too dangerous, i.e., those that kill their host, are not successful since they also die without leaving offspring. Thus, parasites evolve to be minimally harmful to their hosts. The same logic goes for infectious agents – the disease should help propagate the microorganism (e.g, by causing sneezing, diarrhea, etc.) without killing the host.

The organisms that make up ecosystems change over time as the physical and biological structure of the ecosystem changes. Right now, one of the effects of global warming is that some species migrate and others do not. Thus, old ecosystems break down and new ones are formed. The ecosystems are in a process of remodeling. During that process, many species are expected to go extinct.

When an ecosystem is disturbed to some extent, but not completely eradicated, the remodeling process that follows is called primary succession.

When an ecosystem is completely wiped out (e.g,. a volcanic eruption on an island), secondary succession occurs, with a predictable order in which species can recolonize the space. One species prepares the ground (quite literally) for the next one. The process may start with bacteria, lichens and molds, continuing with mosses, fungi, ferns and some insects, etc, finally ending with trees, birds and large mammals. The final structure of the ecosystem is quite stable over time – this is a mature ecosystem.

Previously in this series:

BIO101 – Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype
BIO101 – From Genes To Species: A Primer on Evolution
BIO101 – What Creatures Do: Animal Behavior

BIO101 – What Creatures Do: Animal Behavior

This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

————————————–

Today, we discuss animal behavior. Note that I tend to do a lot of drawing on the whiteboard in this lecture, which is not seen in these notes. I also show a lot of short YouTube videos that show examples of strange animal behaviors.

————————————–

Imagine that you are a zebra, grazing in the savanna. Suddenly, you smell a lion. A moment later, you hear a lion approaching and, out of the corner of your eye, you see the lion running towards you.

What happens next? You start running away, of course. How does that happen? Your brain received information from your sensory organs, processed that information and made a decision to pursue a particular action. That decision is relayed to the muscles that do the actual running.
In short, that is behavior and it can be schematically depicted like this:

Environment———> Sensor ———-> Integrator———> Effector

Here, the change in the environment (appearance of a lion) is perceived by the sensors (eyes, nose, ears), processed by the integrator (the brain) and results in the activity of the effectors (muscles).

But, it is usually not that simple. The flow chart, as depicted, may be accurate when describing behavior of a bacterium, a protist, a fungus or a plant. A molecule in the cell membrane of a bacterium may sense nutrients, toxins or light. This information is processed by the cell as a whole, and as a result, the cilia or flagella move the bacterium in an appropriate direction.

Specialized cells in the shoot-tips or root-tips may detect up and down, or the position of the Sun, and guide growth in an appropriate direction (shoots up, roots down). Sunflowers and some other plants track the position of the Sun throughout the day. Many plants open and close their flowers or leaves at particular times of day. Some flowers, e.g, Venus flytrap and some orchids, can move even faster in order to capture insects.

Pilobolus, a fungus (seen as fine white fuzz on manure), shoots its spores towards the Sun at a particular angle at a particular time of day. Those are all simple behaviors involving a single sensor, a single integrator and a single effector in a simple unidirectional flow of information.

Once we get to animals with central nervous systems, things get a little bit more complicated. There are often multiple sensors. In the zebra example, the changes in environment are detected by three separate sensors: for vision, audition and olfaction. Effectors are many muscles, working in a highly coordinated manner.

Sensors located in the muscles feed the information about their activity back to the integrator. Integrator feeds back to the sensors as well – raising the sensitivity of the sensory organs, including vision, hearing, smell and the tactile sense (touch), while reducing the sensitivity of other sensors, e.g., for pain. The subjective perception of the rate of passage of time slows down, allowing for more fine-grained sensation and faster decision-making by the integrator.

Furthermore, the integrator will stimulate secretion of the hormones which, in turn, may increase the ability of effectors (muscles) to do their work. Integrator will also raise the activity of other organ systems that are important in allowing muscles to perform at their maximal level, e.g., circulatory and respiratory systems that bring oxygen and energy to the muscles.

At the same time, the brain temporarily shuts down the activity of organ systems not necessary for short-term survival, but which may take the valuable energy away from the muscles. Thus, the digestive, immune, excretory and reproductive systems are inhibited.

As the zebra runs away, the act of running results in subsequent changes in the environment, which are again detected by the sensors. The integrator makes decisions to suddenly swerve if the lion gets closer, or to buck and kick if the lion gets very close, or to stop and find the safest route back to the herd if the lion has abandoned the chase.

All the changes described in the zebra example above are elements of the stress response, which is an excellent example of a complex behavior. There are multiple sensors, multiple effectors, various modifications of the body’s physiology, and several kinds of information feedbacks involved. Behavioral biology studies all aspects of it.
In addition, it is not just the activity itself, but also the propensity for such activity that is studied by behavioral biology. Probability of a behavior happening depends on the motivation, or the state of the effector. The state can be modified by hormones, hunger, tiredness, libido, general energy levels, etc. The effector (e.g, the brain) also possesses timing mechanism (clocks and calendars) which make some behaviors much more likely during the day or during the night, some more likely during spring or summer, others more likely during fall or winter.

What Is Behavior?

It is difficult to define behavior without resorting to just listing examples of various kinds of behaviors, but let’s try to define it anyway: Behavior is a change in body’s position, shape or color, or a change in potential for such change, in response to changes in the external or internal environment. Behavior is endogenously generated (i.e., if I move your arm – that is not your behavior, it’s mine), purposive (meant to achieve a goal), and is an evolved adaptation that contributes to survival or reproduction, thus increases one’s fitness (which is obvious in the case of the fleeing zebra).

How to study behavior?

The most informative and profitable way to study behavior is an integrative approach. This means that the behavior under study is approached at all levels of organization (from molecules to ecosystems) and from four different angles. The first angle is Mechanism, which denotes study of the physiology underlying behavior. Most of the analysis of the zebra’s behavior described above focused on this aspect – the physiology of the sensory, neural, muscular and other systems and the way they work together to produce the behavior.

The second one is Ontogeny, the study of embryonic and post-embryonic development of the behavior – how does an individual acquire the behavior, how much is the behavior inherited vs. learned, at what time in one’s life cycle can the behavior be learned or expressed, at what times of day or year are the behaviors most likely to be expressed, etc.

These first two angles – mechanism and ontogeny – are sometimes called Proximate Causes of behavior and are designed to ask and answer the “How” questions of behavior (how does it work, how does it develop). The next two are called Ultimate Causes of behavior and are designed to ask and answer the “Why” questions (why behave in such way).

History is the third approach. It studies the evolutionary history of a behavioral trait, usually by employing the comparative method, i.e., comparison of a number of related species, trying to discover if the behavior is common in all of them, in which case it is present due to the deep phylogenetic history, or of it most reliably varies with the type of environment the species lives in, suggesting that the behavior is a recent adaptation for a particular way of life.

Finally, the fourth approach is Function. It tests the hypothesis that the behavior in question increases the animal’s fitness, aids in survival and/or reproduction, and has evolved for that function – is it an adaptation.

Recently a fifth question has been added to this list. Animal cognition asks “Can animals think?” Here, careful use of some unusual (and quite controversial) methods, including anecdotes, introspection and anthropomorphism, aids in the development of testable hypotheses about the inner worlds of animals.

No other area of biology is as integrative as behavioral biology. It is possible for a biochemist to ignore ecology or for an ecologist to ignore biochemistry (though at the risk of performing irrelevant research), but a behavioral biologist cannot ignore any aspect of the biology of the species under study. This makes the study of behavior the glue that holds all of biology together. This makes behavioral biology difficult to do, as one needs to have strong background in many areas of biology, technical expertise in a broad range of laboratory and field techniques, and lots of time to follow up on the literature in a number of related fields.

Only a few – the best – behavioral biologists are capable of exploring every aspect of a behavior at all levels. Mostly, the problem is divided among a number of laboratories around the world, each researcher using a slightly different approach and different techniques. The laboratories then communicate with each other via formal channels – the publications in scientific journals – and via informal channels – conferences and personal communication (and more recently, on the Web). Thus, a big picture is slowly being built out of its smaller parts, each piece of research being informed by all other pieces of research.

Types of behaviors

Foraging behavior involves finding, catching, handling and ingesting food. It includes the formation and use of feeding territories, learning the hunting techniques, the physiology of hunger, as well as behavioral strategies for avoiding becoming prey.

Animal movement includes, most prominently, long-distance migration including the neural mechanisms of spatial orientation and navigation.

Communication is the ability of animals to communicate information to each other (within and between species) via several sensory channels (or modalities). Those modalities include vision (including infrared, ultraviolet and polarized light, as well as thermoreception), sound (including ultrasound, infrasound and substrate vibrations), chemical signals (smells, pheromones, taste), touch and electrical signals (as in electrical fish).

Reproductive behaviors encompass a broad range of behaviors. Mate-finding, male-male competition, mate-choice and courtship are behaviors involved in securing a mate. Mating behavior ensures fertilization. Nesting and parenting behaviors are meant to ensure the survival of the offspring.

Reproductive behaviors are important elements of evolutionary change. Many phenotypic traits are a result not of natural selection, but of sexual selection, where a trait is selected not by the physical environment but by potential mates. Traits favored by the individuals of the opposite sex tend to be more likely to be passed on to the next generation in that population. This leads to the evolution of exaggerated traits (e.g., the peacock’s tail) and to differences between sexes (e.g., in many bird species the male is brightly colored while the female looks drab).

Mate choice can, potentially, be involved in sympatric speciation, if different individuals in the population favor different traits in their mates, so the gene flow between the two groups gets progressively smaller with each generation. This kind of mating is called assortative mating (as opposed to random mating, where each individual is equally likely to mate with each individual of the opposite sex).

The most common types of mating systems are monogamy, polygyny, and polyandry. A good example of polygyny is the elephant seal in which only one male (after defeating all the other males in one-on-one fights) mates with all the females in his territory.

Polyandry is found only a little less often – one female mates with multiple males over the course of a breeding season, resulting in her offspring being of mixed paternity (i.e., different eggs were fertilized by different males). This has been studied mostly in frogs.

Monogamy is the rarest form of mating strategy in the animal kingdom. A distinction is made between social monogamy and sexual monogamy. Many animals that form breeding pairs, including most species of birds, are engaged in social monogamy – the male and the female build the nest together, mate and raise the chicks together. However, DNA fingerprinting has shown that a small proportion of the eggs is invariably fertilized by a different male – a fleshy neighbor who may not be a good “husband” and “father”, but whose size, bright colors or powerful song indicate other genetic qualities. Thus, some of the progeny of the same female will be fleshy sons, some will be “good husband” sons and some will be daughters – the female is hedging her bets about the production of grandoffspring.

Humans are not officially classified as monogamous animals – though human polygamy (both polygyny and polyandry) tends to be in the form of serial monogamy, i.e., sticking monogamously with one partner for a particular length of time, then changing the partner. Social norms have strongly opposed, but did not eradicate human non-monogamy. Increased life-span, invention of reliable contraception, and economic independence of women are making it more and more difficult to suppress the non-monogamous tendencies in humans, as seen from statistics for divorce (around 50%), re-marrying, and cheating (around 60% of both men and women) that have held quite steady over the past 50 years or so.

Social behaviors involve relationships between individuals of the same species. Some animals tend to live alone, each individual defending a territory, and a male and a female meeting only briefly during the mating season. Other animals tend to live in smaller or larger groups. Some animals change their social structure seasonally – for instance, European quail live in coveys (10-12 birds) during the winter), in huge flocks during spring and fall migrations, and in breeding pairs during summer.

Within groups, there is often a hierarchy of individuals – the so-called “pecking order”. The social hirearchy is established through aggression, often in form of ritualized displays. In many species, the ritualized aggressive behaviors are so-called “fixed-action patterns“, i.e., a strongly heritable order of particular movements. Mating behaviors are also often fixed-action patterns.

In some species, the mating fixed-action patterns are also used for aggressive encounters. In some cases, when a male mounts another male utilizing a typical mating pattern, this is actually a display of social dominance. However, in other species, a male mounting a male is actually homosexual behavior, evolved not to determine social hierarchy, but quite the opposite, to increase social coherence within the group (“making friends”). In pygmy chimps (bonobos), everyone in a troop mates with everyone else in the troop, regardless of gender. This makes the troop socially cohesive (which helps in group’s defense if attacked by another troop, predators or other enemies).

Previously in this series:

Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype
BIO101 – From Genes To Species: A Primer on Evolution

#Arseniclife link collection

Native arsenic, by Aram Dulyan at Wikimedia Commons.

Over the past year or so I have been diligently collecting all the links related to the (in)famous #arseniclife affair at my old blog. Links are, especially later in the process, more or less in the chronological order. I guess it will be easier for me to update, and easier for people to find it, if I re-post it here:

Mono Lake bacteria build their DNA using arsenic (and no, this isn’t about aliens) and Science gets it (mostly) wrong again: My take on the NASA astrobiology paper and Lots of Ink for a few extremophiles: We’ve been invaded by aliens, Monolakians, from the Duncecap Galaxy and When life gives you arsenic, make arsenate-backboned DNA, non-alien Halomonadaceae!

Preliminary Thoughts on the “Arsenic-Based Life” Paper and Ordinary evidence would do

The Real Scoop on Aliens Oops Arsenic in Old Lakes and Bacteria Use Arsenic As Basic Building Block In A Pinch and Poison Nil: Mono Lake Bacterium Exhibits Exotic Arsenic-Driven Biological Activity and Arsenic and Odd Lace and It’s not an arsenic-based life form.

Arsenic and Old Lakes: NASA Finds Life NOT As We Know It and Arsenic-Eating Bacteria Expands Definition of Life and It Came From Mono Lake and Complete heresy: life based on arsenic instead of phosphorus and Bacteria eat arsenic – and survive!

Arsenic-associated bacteria (NASA’s claims) and Arsenic-permissive bacteria – implications for arsenical cancer chemotherapy and Are there viruses of arsenic-utilizing bacteria? and The ‘Give Me a Job’ Microbe

Of Arsenic and Aliens and NASA’s real news: bacterium on Earth that lives off arsenic! and Close Encounters of the Media Kind and A Life Less Ordinary and Life With Arsenic: Who’d Have Thought? and Medicine! Poison! Arsenic! Life itself!

Why “alien” life, aka arsenic-loving bacteria, embargo fiasco was deja vu for Sun Spaceman Paul Sutherland and Did you know you could have bet on the NASA arsenic-based bacteria find? and On science blogs this week: Alien abductions and Nasa dismisses criticism of ‘arsenic bacteria’ research

Arsenic-Eating Bacteria May Not Redefine Life, But Could They Be Useful in Oil Spill Cleanup? and A new life form? Not so fast and Arsenic and Old Lace and Arsenic-Based Life

The Wrong Stuff: NASA Dismisses Arsenic Critique Because Critical Priest Not Standing on Altar and NASA: science shouldn’t be debated in media and blogs?! and Not getting it and “This Paper Should Not Have Been Published”: Scientists see fatal flaws in the NASA study of arsenic-based life.

Unquestioning dogma: the gatekeepers of science and Death for “Arsenic-Based Life”? and My summary of NASA’s arsenic-thriving bacteria story and Arsenic and Bacteria: “nothing in that paper is going into my biochemistry textbook” and Why was #PLoS ONE blamed for the media hype about the Darwinius and Red Sea papers, but when it comes to the latest overblown #Science paper, it is #NASA that’s blamed for the hype? (same applies to Venter’s synthetic life: Venter gets the blame not Science) and Heavy Metal

And the skeptics keep chiming in…George Cody on arsenic life and NASA discovers life on Earth and Extraordinary claims attract extraordinary blogging and The Value of Blogs and Ordinary evidence would do

[guest post: Alex Bradley, PhD] Arsenate-based DNA: a big idea with big holes and On how science happens – Case Study: NASA, Arsenic, and Controversy and Is That Arsenic-Loving Bug — Formerly an Alien — a Dog?

Hat die NASA Aliens gefunden? (natürlich nicht) and Die Arsen-Bakterien: Doch ein lohnendes Forschungsobjekt? and Science Is Sexy: Why Do NASA’s New Arsenic Bacteria Matter? and NASA’s arsenic microbe science slammed and Inside scoop from the NASA man who was way ahead of the rest of NASA on those Mono microbes with arsenic in their genes.

NASA’s new life form: Underwhelming? and Did NASA really find new life? and NASA’s Arsenic-Eating “Alien” Bacteria Is More Like Science-Fiction and Was NASA’s big announcement a big mistake? and NASA’s Arsenic-Loving Bacteria Don’t Love Arsenic After All, Critics Say.

An arsenic bacteria postmortem: NASA responds, tries to pit blogs vs. “credible media organizations” and The Right Place for Scientific Debate?: Scientists snub media as controversy over arsenic-eating microbes rolls on and Hey, NASA: this is what peer review actually looks like.

The dubious arsenic bacterium and Life on Arsenic? and NASA arsenic story – let’s lay off the personal attacks on all sides and Scientific dissention: shouldn’t we all be nice? and Arsenic about face and My Letter to Science and DNA, Phosphorus, and Arsenic and NASA can’t have it both ways.

Wolfe-Simon et al Comment: 08 December 2010 and Scientists: NASA’s claim of microbe that can live on arsenic is ‘flawed’ and Did NASA follow its own code of conduct in announcing the arsenic bacteria study? (Hint: No) and Post-publication peer review in public: poison or progress?

Of arsenic and aliens: What the critics said and Falsehoods associated with the arsenic-thriving bacteria story: What it is and what it isn’t and Critics raise doubts on NASA’s arsenic bacteria and Three Tales of Arsenic Tolerant Bacteria

Robert Sheldon, ID proponent, defending the arsenic bacteria paper? Oh dear God. and Arsenic Bacteria Breed Backlash and Don’t Like Arsenic Bacteria? Put Your Experiment Where Your Mouth Is! and GFAJ-1: Get Fighting And Jousting! and Albert Eschenmoser and I Had Arsenic for Lunch

Arsenic bacteria – a post-mortem, a review, and some navel-gazing and Of Arsenic, Slime Molds, and Life on Other Worlds and On science blogs this week: Arsenic bugging and Science Weekly: The arsenic bacterium that could help find life in outer space

Aliens, arsenic and alternative peer-review: Has science publishing become too conservative? and Arsenic up for Review and Arsenate redux and No-one cuts deeper than a Science Blogger. and Your daily dose of arsenic: On the Madeleine Brand Show on KPCC

The Agency That Cried “Awesome!” and Arsenic and Primordial Ooze: A History Lesson and Poisoned Debate Encircles a Microbe Study’s Result and How to harness distributed discussion of research papers and Molecular evolution of an arsenate detoxification pathway by DNA shuffling

If a Microbe Can Do It…: Finding Happiness Even Amid Toxicity (this one is total crap, but what do you expect from HuffPo)

Science Weekly: The great arsenic bacteria backlash and Good Science or good publicity? and Arsenic And Peer Review and Communication – it’s not just for cells and MEDIA ADVISORY: M10-167 and Ambitions of an Early Career Scientist? and Scientific knowledge – getting closer to the right answer

Where can we find arsenic in a DNA structure? and Not Exactly Rocket Science etc -The Great Monolakian Arsenic Issue and its quick rise to fame and flame and The Arsenic Chronicles and In Search of Life: SETI has come a long way over the years, but is the search really important? and Just to be clear: Ed Yong does read the primary literature

Calling Dr. Kane and A new kind of life? and Response required and More on Arsenic Bugs – Nature responds to the blogosphere

The arsenic post I never wrote and What Alien Bacteria Can Teach Us About Health PR and Response to Questions Concerning the Science Article, A Bacterium That Can Grow by Using Arsenic Instead of Phosphorous (PDF) and Real science – warts and all

Arsenic bacteria study authors respond to critics and Using the ‘arsenic bacteria’ story as a teaching moment for undergraduates

A Funny Arsenic Smell Upstream — What questions is it fair to ask about squishy science? and Comments on Dr. Wolfe-Simon’s Response and Yet another reason why the Wolfe-Simon conclusion is so improbable and Arsenic and Old Wounds

Scientists and the News Media: Arsenic-Based Life Forms a Case Study? and Arsenic Bacteria 4: The Quest for Peace and Confused about Arsenic

Exclusive Interview: Discoverer of Arsenic Bacteria, in the Eye of the Storm and #ArsenicLife #Fail: A teachable moment and Response to the critics.

Phosphorus beats arsenic…by a factor of seventeen powers of ten and An arsenic-laced bad-news letter: Who is the audience for online post-publication peer review?

Added four months later:
Arsenic life, four months later: pay no attention to the internet and Arsenic life, four months (and a bit) later: Reviewers with shovels and Comment posted on Rosen paper and Response from Drs. McDermott and Rosen about their arsenic paper and Arsenic Author Dumps Peer Review, Takes Case to TED and Felisa Wolfe-Simon (of arsenic infamy) is no more convincing in person than in print

And another couple of months later:

Science Publishes “Arsenic is Life” Critiques. Game On., Arsenic, RNA, and the unpleasant aftertaste of hype, The Discovery of Arsenic-Based Twitter, “The Center of Gravity Has Shifted.” Carl Zimmer on the Arsenic Paper, Critics weigh in on arsenic life.

Arseniclife: The formal critiques and the authors’ responses, Wolfe-Simon et al.’s responses to my comments, How to test the arsenic-DNA claims, How might a bacterium evolve to use arsenic in place of phosphorus?.

Arsenic-based bacteria: Fact or fiction?, Critics take aim at NASA ‘arsenic life’ study, Debate over arsenic-based life enters a new chapter, Science Publishes Multiple Critiques of Arsenic Bacterium Paper

#arseniclife, peer review, and the scientific process, High Impact Science in a Hyperactive Media Environment, Arsenic life – more criticism, formally published, Post publication peer review – a new way of doing science?.

Were my original #arseniclife criticisms overly personal?, Examples of good astrobiology please, Further panning of the arsenic life claims, Minding the As and P: Can Arsenic Substitute for Phosphorus or Not?.

What the Coburn report has in common with arsenic life, Finding the truth is a waste of time, scientists say, Does Arsenic Really Exist in the DNA from GFAJ-1?, The Arsenic Paper is out, along with eight critiques.

Return of the Arsenic Bacterium, Felisa Wolfe-Simon Does NOT Get It, Arsenic-based life debate continues, Follow arsenic life science “live”.

From the shadows to the spotlight to the dustbin – the rise and fall of GFAJ-1, Arsenic bacteria have changed science…science education that is.

Just in case I do decide to test the #arseniclife …, Working safely with arsenic (what I’d need to know), Guest post about #arseniclife, Starting to work with GFAJ-1!, They’re here!, Counting the GFAJ-1 cells, Vitamins are for wusses (#arseniclife), Why would GFAJ-1 grow much better on agar than in liquid?, Maybe it’s the water? Or the tubes?

It’s not the water, nor the tubes, nor the parafilm…, No excuses… , More detailed plans, GFAJ-1 (no real progress to report), Life and death of GFAJ-1…. and many more posts detailing the process of replicating the research.

Scientist in a Strange Land and Arsenic is Life and the View From Nowhere and #ArsenicLife Goes Longform, And History Gets Squished and Tom Clynes on arsenic life.

Arsenic, quasicrystals and the myth of the science martyr

BIO101 – From Genes To Species: A Primer on Evolution

This post was originally written in 2006 and re-posted a few times, including in 2010.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

Today, we introduce the concept of evolution, mainly via natural selection (sexual selection will come later in the course, and neutral selection etc. are too much for this level). Note that I tend to do a lot of drawing on the whiteboard in this lecture, which is not seen in these notes.

———————————————————-

Evolution

Imagine a small meadow. And imagine in that meadow ten insects. Also imagine that the ten insects are quite large and that the meadow has only so much flowers, food and space to sustain these ten individuals and not any more. Also imagine that the genomes of those ten insects are identical, except for one individual: that one has a mutation in one gene (due to an error in DNA replication, or due to crossing-over during meiosis, or due to chemicals in the environment, or due to getting hit by rays coming from outside Earth, etc). That mutation, during development, led to the induction of the production of more mitochondria in each muscle cell.

Normally, that mutation is not obvious – the insect flutters from flower to flower just like anyone else. However, if the situation arises, the mutant individual is just a tiny little bit faster because the additional mitochondria in muscles allow it to switch from aerobic to anaerobic sources of energy later than in other individuals. Thus, the “normal” individuals can fly one yard in one second, while the mutant can fly one yard plus one inch in one second.

Now imagine that, over some time period, a bird comes by the meadow four times. Each time, the bird chases the insects and catches the one that is the closest to her. Which individual is, statistically speaking, least likely to get caught and eaten? The mutant, as the little extra speed may give it just enough edge in comparison to other individuals. This comparative “extra edge” is called increased fitness.

After four insects have been eaten, six remain – three males and three females. They pair up, mate, lay eggs and die. Each pair lays, let’s say eight eggs, which all hatch, proceed normally through the larval development and become adults. This makes a total of 24 insects in a meadow that can support only ten individuals. At the same time, the bird has laid eggs, the eggs hatched and the hatchlings sometimes come to the meadow to hunt.

Let’s look at the genetics of this population for a moment. Two pairs of “normal” insects produced a total of 16 offspring, all of them “normal”. The offspring of one “normal” and one “mutant” each got one of the chromosomes from the mother, the other one from the father. All of them will have the mutation on one, and not on the other chromosome. Let’s say that having a mutation on only one chromosome adds a half-inch to the yard-per-second flaying speed. The full mutant is homozygous for this mutation. The half mutant is heterozygous for this mutation. The heterozygous individuals are still relatively more fit than the “normals”. As the hatchling birds hunt down the insects and cut down the population to ten individuals, the half-mutants are more likely to be present in the remaining population than the non-mutants.

Let’s call the “normal” variant of the gene A and the “mutant” variant of the same gene a. A and a are alleles of the same gene.

In the next generation, some normals will breed with normals, producing normal offspring. Some half-mutants will mate with normals and produce a mix of normals and half-mutants. Some half-mutants will mate with some half-mutants and the resulting eight offspring will consist of 2 normals (AA), two mutants (aa), and four semi-mutants (Aa).

As the a allele confers relative fitness to its carriers, this allele will spread through the population over several generations and either completely eliminate allele A, or attain some stable balanced ratio in the population.

When one compares the genetic composition of this population over generations, one notices that it changes over time, from preponderance of A in the first generation, through a series of intermediate stages, to the preponderance of a in the last generation.

The change of genetic composition of a population over multiple generations is called evolution.

That sentence is the most commonly used definition of evolution. The process that favored one allele over the other, resulting in evolution of flight speed in these insects, is called natural selection. The environment – the carrying capacity of the meadow plus the bird predators – was the selecting agent. The process that turns a genetic change (mutation) into a trait that can affect fitness of the whole organism is development. Thus, one can also define evolution as “change of development by ecology”.

For evolution to proceed, the trait must vary in a population, one of the variants has to confer greater fitness than the other variants, there has to be a limit on the fecundity (how many offspring can survive in each generation) leading to differential rate of reproduction, and the trait has to be heritable, i.e., the offspring have to be more like parents in respect to that trait than like other individuals in the population. The inheritance is usually, though not always, conferred by the genome (the DNA sequence).

The example we used is quite unrealistic. Populations are much more likely to number in thousands or millions than just ten individuals. Thus, instead of a few generations, it may take thousands or millions of generations for a new allele to sweep through the population. In annually breeding organisms, this means thousands to millions of years. In slow-breeding animals, like elephants, it will take even longer. In fast reproducers, like bacteria, this may only take several months or years, as in evolution of antibiotic resistance in bacteria or evolution of pesticide resistance in agricultural pests.

Another way that the example was unrealistic was the assumption that all the individuals were genetically identical to each other except for that one mutation in that one gene. In reality, there will be variation (two or more alleles) in every gene, and new mutations show up all the time. Some mutations decrease fitness, some are neutral and some increase fitness. Some alleles affect fitness depending on which other alleles of other genes are present in the same individuals, or depending on the environment it finds itself in at a particular time, as in the ‘norm of reaction’ phenomenon (see previous lecture). Due to this, some combinations of alleles may tend to move from one generation to the next together.

Finally, in many organisms, genes can be transmitted horizontally – not from parent to offspring but directly from one individual to another. This most often happens in bacteria, where individual bacteria may exchange bits and pieces of their DNA. Likewise, viruses are carriers of DNA sequences from one organism to another as well. Some of the sequences in our genome are of bacterial origin, transmitted some time in the past by viruses, and now fully integrated into our genome and even assuming an indispensable function. For instance, HERV genes are originally viral genes that are now parts of our genome and are necessary for the development of the placenta.

Thus, in the real world, the situation is more complicated than in our example. Still, the proportions of various alleles of many genes are constantly changing in populations over generations – evolution occurs all the time.

Let’s now assume that our insects live in a much larger area and that there are millions of them. The frequencies of various alleles fluctuate all the time, and there is quite a lot of genetic variation contained in the population. Natural selection may work on preserving the average phenotype as its fitness is high and outliers at each end have lower fitness. This is called stabilizing selection.

As the climate slowly changes, or other aspects of the environment change, the relative frequencies of alleles of various genes will track those changes. New conditions may, for instance select for larger body size. The largest individuals tend to leave most offspring, while the smallest individuals, on average, put the least of their genes into the next generation. The selection for large body size is an example of directed selection.

In some cases, selection may favor the extremes, but not the middle. Fast fliers may be selected for because they can escape the birds. The slowest fliers may be selected because they mostly walk or crawl and are thus not easily spotted by birds. They are also fit, but via a different strategy. The medium-speed fliers are selected against. This is an example of disruptive selection, forming two different morphs of the same species.

If those two morphs tend to, on average, be more likely to find each other and mate with each other within a morph than between two morphs, this may lead to splitting the species into two species – this is called sympatric speciation. As the gene flow between the two groups declines, more and more mutations/alleles will be found only in one morph and not the other. Those genes will also be under the influence of selection, and the selecting environment is different between crawlers and fliers. Soon enough, the individuals belonging to the two groups will not even recognize each other as belonging to the same species. Even if they recognize each other, they may not like each other (“mate-choice”) enough to mate. Even if they mate, their eggs may not be fertile. Even if their eggs are fertile, the resulting offspring may not be fertile (hybrids, like mules for instance). If, for whatever reason, two related populations do not, will not or cannot interbreed, they have became separate species – speciation occurred.

Imagine now that a small cohort of about ten individuals got blown away by wind from the mainland to a nearby island. The mainland population is huge. The island population is tiny. The ability of any mutation or any allele to spread fast through the population is much greater in a small group. The selective pressures are also different.

It may be better for the island insects to be small and for the mainland insects to be large, perhaps due to the types of flowers or kinds of predators that are present. The mainland insects may be selected for high flying speed because of bird predation. The island insects may not have any bird predators, but, those individuals who are the best fliers are most likely to be swept off the island by wind and drown in the ocean, never placing their genes into the next generation. Thus, they are selected not to fly, even to lose their wings.

If, after a number of generations, those two populations again get into contact – e.g., a land bridge gradually arises, or another cohort of mainland insects floats on a log onto the island, the two populations will not recognize each other as the same species (or not like each other enough to mate, or not having fertile eggs or offspring). Thus, they have also become reproductively isolated, thus, by definition, they have become two separate species. Speciation occurred. This type of speciation, where a geographic barrier separates two parts of a population preventing gene flow between them is called allopatric speciation, and is much better documented and much less controversial than sympatric speciation.

Billions of such speciation events, meaning branching of species into two or more species, resulted in the evolution of all species of organisms on Earth from a single common ancestor (a very primitive bacterium) over a period of more than 3.5 billion years.

Watch animation:

Evolution

Further readings:

Understanding Evolution
What is Evolution?
Introduction to Evolutionary Biology
Evolution FAQs
Index to Creationist Claims
Talk Design Articles
Talk Reason
Transitions

Previously in this series:

Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development
BIO101 – From Genes To Traits: How Genotype Affects Phenotype

The Mighty Ant-Lion

First written on March 04, 2005 for Science And Politics, then reposted on February 27, 2006 on Circadiana, and re-posted a few more times as I moved my blog around (the latest in 2009) a post about a childrens’ book and what I learned about it since.

When I was a kid I absolutely loved a book called “Il Ciondolino” by Ricardo Vamba – a book in two slim volumes for kids (how times change – try to publish a 200+ page book of dense text for children today!). I later found out that it was translated into English under the title The Prince And His Ants in 1910 (Luigi BERTELLI (M: 1858 or 1860 – 1920) (&ps: VAMBA) The Prince And His Ants [It-?]. Holt.(tr S F WOODRUFF) [1910] * Il Giornalino Di Gran Burrasca [It-?] (tr ?) [?] ) and was even The Nation’s Book of the Week on June 2nd 1910.

[“Vamba” is the pseudonym of Italian fantasist Luigi Bertelli. The Prince and His Ants (1910) tells the tale of a boy who becomes an ant, and a girl who becomes a butterfly. The English translation by one Miss Woodruff was edited by Vernon Kellogg, an insect authority at Stanford University. Ninety interior illustrations are scientifically accurate.]

This book is hard to find – don’t even bother with Amazon – but my brother was persistent and after several weeks of patient searching he got a copy from Alibris and sent it to me. It is a story of a boy who wakes up one morning transformed into an ant. The book describes his travels and adventures in the world of the small. Of course, he meets a bunch of really cool creatures, like various wasps, and bees, and moths, and honey-ants, etc. But the one I remember the most was the ant-lion.

Photo by Jonathan Numer at Wikimedia Commons.

The antlion is actually quite pretty, yet short-lived, as an adult. But it is the larva that is really cool:

It digs a pit in the sand and hides underneath the sand right under the bottom of the pit. When an ant or some other insect comes by, it falls into the pit and has trouble climbing out of its steep walls again. The ant-lion lunges out of the sand (like a scene from “Tremors”) and eats the poor bug:


Now the really cool part: the volume of the pit is bigger when the antlion is hungrier (or so they say at this marvelous website that I highly recommend you browse around). But, hungry or not, the ant-lion digs a bigger pit when the moon is full. Nobody has any idea why that would be so. Here is a photograph (from the site I linked in the previous sentence) of a colony of ant-lions, each with its own little pit:


But here is the coolest part of all. If you take ant-lions out of the field and put them in little sandboxes in the laboratory and isolate them from any cues about the outside world they will still dig bigger pits roughly every four weeks – they have an internal lunar rhythm:


They have, somewhere in their brains, a lunar clock that tells them to dig larger pits whenever the moon is full even if they canot see the moon itself (e.g., on a dark cloudy night). If and when somebody figures out how this little brain works, I’ll be sure to tell you, but you may have to wait years for it – I don’t think anybody is even thinking about studying it right now.

References:

G.J. Youthed, V.C. Moran, The lunar-day activity rhythm of myrmeleontid larvae, Journal of Insect Physiology,Volume 15, Issue 7, July 1969, Pages 1259-1271

Inon Scharf, Aziz Subach, Ofer Ovadia, Foraging behaviour and habitat selection in pit-building antlion larvae in constant light or dark conditions, Animal Behaviour, Volume 76, Issue 6, December 2008, Pages 2049-2057 (PDF)

 

BIO101 – From Genes To Traits: How Genotype Affects Phenotype

This post was originally written in 2006 and re-posted a few times, including in 2010. Please help me locate the sources of the images – I assume they are from the text book I used at the time, but am not completely sure.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

Today, I tackle the important but difficult task of explaining why “gene for” idea is wrong and how to think in a more sophisticated manner about the way genes affect phenotype.

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How Genotype Affects Phenotype

One often hears news reports about discoveries of a “gene for X”, e.g., gene for alcoholism, gene for homosexuality, gene for breast cancer, etc. This is an incorrect way of thinking about genes, as it implies a one-to-one mapping between genes and traits.

This misunderstanding stems from historical precedents. The very first genes were discovered decades ago with quite primitive technology. Thus, the only genes that could be discovered were those with large, dramatic effects on the traits. For instance, a small mutation (change in the sequence of nucleotides) in the gene that codes for RNA that codes for one of the four elements of the hemoglobin protein results in sickle-cell anemia. The red blood cells are, as a result, misshapen and the ability of red blood cells to carry sufficient oxygen to the cells is diminished.

Due to such dramatic effects of small mutations, it was believed at the time that each gene codes for a particular trait. Today, it is possible to measure minuscule effects of multiple genes and it is well understood that the “one gene/one trait” paradigm is largely incorrect. Most traits are affected by many genes, and most genes are involved in the development of multiple traits.

A genome is all the genetic information of an individual. Each cell in the body contains the complete genome. Genomes (i.e., DNA sequences) differ slightly between individuals of the same species, and a little bit more between genomes of closely related species, yet even more between distantly related species.

Exact DNA sequence of an individual is its genotype. The collection of all observable and measurable traits of that individual is phenotype.

If every position and every function of every cell in our bodies was genetically determined, we would need trillions of genes to specify all that information. Yet, we have only about 26,000 genes. All of our genes are very similar to the equivalent genes of chimpanzees, yet we are obviously very different in anatomy, physiology and behavior from chimpanzees. Furthermore, we share many of the same genes with fish, insects and even plants, yet the differences in phenotypes are enormous.

Thus, it follows logically that the metaphor of the genome as a blueprint for building a body is wrong. It is not which genes you have, but how those genes interact with each other during development that makes you different from another individual of the same species, or from a salmon or a cabbage.

But, how do genes interact with each other? Genes code for proteins. Some proteins interact with other proteins. Some proteins regulate the transcription or replication of DNA. Other proteins are enzymes that modify other chemicals. Yet other proteins are structural, i.e., become parts of membranes and other structures.

A slight difference in the DNA sequence will have an effect on the sequence of RNA and the sequence of the resulting protein, affecting the primary, secondary and tertiary structure of that protein. The changes in 3D shape of the protein will affect its efficiency in performing its function.

For instance, if two proteins interact with each other, and in order to do so need to bind each other, and they bind because their shapes fit into each other like lock and key, then change of shape of one protein is going to alter the efficiency of binding of the two. Changes in shapes of both proteins can either slow down or speed up the reaction. Change of rate of that one reaction in the cell will have effects on some other reaction in the cell, including the way the cell reacts to the signals from the outside.

Thus genes, proteins, other chemicals inside the cell, inter-cellular interactions and the external environment ALL affect the trait. Most importantly, as the traits are built during development, it is the interactions between all these players at all levels of organizations during development that determine the final phenotype of the organism.

The importance of the environment can be seen from the phenomenon of the norm of reaction. The same genotype, when raised in different environments results in different phenotypes. Furthermore, different genotypes respond to the same environmental changes differently from each other. One genotype may produce a taller plant at higher elevation while a slightly different genotype may respond quite the opposite: producing a shorter plant at higher elevations.


So, if genes do not code for traits, and the genome is not a blueprint, what is the best way to think about the genome and the genotype/phenotype mapping? I have given you handouts (see below) with four different alternative metaphors, at least one of which, I hope, will feel clear and memorable to each student. I will now give you a fifth such metaphor, one of my own:

Imagine that a cell is an airplane factory. It buys raw materials and sells finished airplanes. How does it do so? The proteins are the factory workers. Some of them import the materials, others are involved in the sale of airplanes. Some guard the factory from thieves, while others cook and serve food in the factory cafeteria.

But the most important proteins of this cell are those that assemble the parts of airplanes. When they need a part, e.g., a propeller, they go to the storeroom (nucleus) and check the Catalogue Of Parts (the DNA), and press the button to place an order for a particular part. Other proteins (storeroom managers) go inside and find the correct part and send it to the assembly floor (endoplasmic reticulum).

But, protein workers are themselves robots assembled out of parts right there in the same factory, and the instructions for their assembly are also in the Catalogue of Parts (DNA) in the nucleus.

Further reading:

How do you wear your genes? (PDF) by Richard Dawkins.
An analogy for the genome by Richard Harter.
It’s not just the genes, it’s the links between them by Paul Myers
PZ Myers’ Own Original, Cosmic, and Eccentric Analogy for How the Genome Works -OR- High Geekology by Paul Myers
It’s more than genes, it’s networks and systems by Paul Myers.

Previously in this series:

Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication
BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development

BIO101 – From Two Cells To Many: Cell Differentiation and Embryonic Development

This post was originally written in 2006 and re-posted a few times, including in 2010. Please help me locate the sources of the images – I assume they are from the text book I used at the time, but am not completely sure.

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

 

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Cell Differentiation and Embryonic Development
BIO101 – Bora Zivkovic – Lecture 2 – Part 2
There are about 210 types of human cells, e.g., nerve cells, muscle cells, skin cells, blood cells, etc. Wikipedia has a nice comprehensive listing of all the types of human cells.

What makes one cell type different from the other cell types? After all, each cell in the body has exactly the same genome (the entire DNA sequence). How do different cells grow to look so different and to perform such different functions? And how do they get to be that way, out of homogenous (single cell type) early embryonic cells that are produced by cell division of the zygote (the fertilized egg)?

The difference between cell types is in the pattern of gene expression, i.e., which genes are turned on and which genes are turned off. Genes that code for enzymes involved in detoxification are transcribed in lver cells, but there is not need for them to be expressed in muscle cells or neurons. Genes that code for proteins that are involved in muscle contraction need not be transcribed in white blood cells. The patterns of gene expression are specific to cell types and are directly responsible for the differences between morphologies and functions of different cells.

How do different cell types decide which genes to turn on or off? This is the result of processes occurring during embryonic development.

The zygote (fertilized egg) appears to be a sphere. It may look homogenous, i.e., with no up and down, left or right. However, this is not so. The point of entry of the sperm cell into the egg may provide polarity for the cell in some organisms. In others, mother may deposit mRNAs or proteins in one particular part of the egg cell. In yet others, the immediate environment of the egg (e.g., the uterine lining, or the surface of the soil) may define polarity of the cell.

When the zygote divides, first into 2, then 4, 8, 16 and more cells, some of those daughter cells are on one pole (e.g., containing maternal chemicals) and the others on the other pole (e.g., not containing maternal chemicals). Presence of chemicals (or other influences) starts altering the decisions as to which genes will be turned on or off.

As some of the genes in some of the cells turn on, they may code for proteins that slowly diffuse through the developing early embryo. Low, medium and high concentrations of those chemicals are found in diferent areas of the embryo depending on the distance from the cell that produces that chemical.

Other cells respond to the concentration of that chemical by turning particular genes on or off (in a manner similar to the effects of steroid hormones acting via nuclear receptors, described last week). Thus the position (location) of a cell in the early embryo largely determines what cell type it will become in the end of the process of the embryonic development.

The process of altering the pattern of gene expression and thus becoming a cell of a particular type is called cell differentiation.

The zygote is a totipotent cell – its daughter cells can become any cell type. As the development proceeds, some of the cells become pluripotent – they can become many, but not all cell types. Later on, the specificity narrows down further and a particular stem cell can turn into only a very limited number of cell types, e.g., a few types of blood cells, but not bone or brain cells or anything else. That is why embryonic stem cell research is much more promising than the adult stem cell research.

The mechanism by which diffusible chemicals synthesized by one embryonic cell induces differentiation of other cells in the embryo is called induction. Turning genes on and off allows the cells to produce proteins that are neccessary for the changes in the way those cells look and function. For instance, development of the retina induces the development of the lens and cornea of the eye. The substance secreted by the developing retina can only diffuse a short distance and affect the neighboring cells, which become other parts of the eye.

During embryonic development, some cells migrate. For instance, cells of the neural crest migrate throughout the embryo and, depending on their new “neighborhood” differentiate into pigment cells, cells of the adrenal medula, etc.

Finally, many aspects of the embryo are shaped by programmed cell death – apoptosis. For instance, early on in development our hands look like paddles or flippers. But, the cells of our fingers induce the cell death of the cells between the fingers. Similarly, we initially develop more brain cells than we need. Those brain cells that establish connections with other nerve cells, muscles, or glands, survive. Other brain cells die.

Sometimes just parts of cells die off. For instance, many more synapses are formed than needed between neurons and other neurons, muscles and glands. Those synapses that are used remain and get stronger, the other synapses detach, and the axons shrivel and die. Which brain cells and which of their synapses survive depends on their activity. Those that are involved in correct processing of sensory information or in coordinated motor activity are retained. Thus, both sensory and motor aspects of the nervous system need to be practiced and tested early on. That is why embryos move, for instance – testing their motor coordination. That is why sensory deprivation in the early childhood is detrimental to the proper development of the child.

The details of embryonic development and mechanisms of cell differentiation differ between plants, fungi, protists, and various invertebrate and vertebrate animals. We will look at some examples of those, as well as some important developmental genes (e.g., homeotic genes) in future handouts/discussions, and will revisit the human development later in the course.

Previously in this series:

Biology and the Scientific Method
BIO101 – Cell Structure
BIO101 – Protein Synthesis: Transcription and Translation
BIO101: Cell-Cell Interactions
BIO101 – From One Cell To Two: Cell Division and DNA Replication

 

Everything You Always Wanted To Know About Sleep (But Were Too Afraid To Ask)

This post is by far, my most popular ever. Sick and tired of politics after the 2004 election I decided to start a science-only blog – Circadiana. After a couple of days of fiddling with the template, I posted the very first post, this one, on January 8th, 2005 at 2:53 AM and went to bed. When I woke up I was astonished as the Sitemeter was going wild (getting a couple of thousand hits was a big deal back then, but within a few days, this post got to about 60,000 visits)! This post was linked by BoingBoing and later that day, by Andrew Sullivan. It has been linked by people ever since, rediscovered over and over again, although the post is six and a half years old.
I decided to move the post from the old archives here without any editing. I hope my writing has improved since then. And beware that it is more than six years out of date. It is here, really, to show my first real scienceblogging post, the one that convinced me, due to positive response, to switch from political to science blogging. A piece of personal history, if you wish.

What are you doing up so late, staring at the computer screen reading this? For that matter, what am I doing up late writing this at 11pm? Are we all nuts?

Until not long ago, just about until electricity became ubiquitous, humans used to have a sleep pattern quite different from what we consider “normal” today. At dusk you go to sleep, at some point in the middle of the night you wake up for an hour or two, then fall asleep again until dawn. Thus there are two events of falling asleep and two events of waking up every night (plus, perhaps, a short nap in the afternoon). As indigenous people today, as well as people in non-electrified rural areas of the world, still follow this pattern, it is likely that our ancestors did, too.The bimodal sleep pattern was first seen in laboratory animals (various birds, lizards and mammals) in the 1950s, 60s and 70s, i.e, before everyone moved their research to mice and rats who have erratic (un-consolidated) sleep patterns. The research on humans kept in constant conditions, as well as field work in primitive communities (including non-electrified rural places in what is otherwise considered the First World) confirmed the bimodality of sleep in humans, particularly in winter.

Larks and Owls
There is a continuum of individual sleep patterns ranging from extreme “larks” who fall asleep at the first inkling of dusk but wake up before dawn, all the way to the extreme “owls” who stay up quite late and wake up once the day is in full swing, and of course everything in between. No matter where you are on this continuum, you tend to sleep more during the winter long nights than during the short summer nights.

The genetic basis of extreme “larkiness” has been elucidated. It is a mutation in a phosphorilation site on the protein product of the core-clock gene period (per). A phosphorilation site on a protein is a place where another protein may add a phosphate group. Phosphate groups are ubiquitous sources of energy in biology (remember ATP from high-school biology? That’s it!). Thus, an addition of the phophate may make it easier for the protein to react with another molecule. That other molecule may give it stability, or destroy it, or allow it to move to another part of the cell. In the case of period, it appears that lack of the phosphate group allows the protein to move into the nucleus sooner than normal where it blocks transcription of its own gene.

Of course, we are talking statistics here: hundreds or thousands of period proteins per cell, several thousand pacemaker clock-cells in the suprachiasmatic nuclei, plus trillions of peripheral clock-cells all over the body: each of these molecules has a statistical chance of moving back into the nucleus sooner than in a person without a mutation. Moving sooner into the nucleus means that the inherent (“freerunning”) period of the clock is shorter. In most people it is about 24-25 hours long (when measured in completely constant environmental conditions, i.e., no light-dark, temperature, sound, or social cycles). The “owls” have longer periods and “larks” have shorter periods. Period determines phase relationship between the internal clock and the environmental synchronizing cue (e.g., the light-dark cycle), thus longer the period of the clock, later the clock will trigger waking up in the morning or feeling sleepy in the evening, and vice versa. People like me go to bed at 4am and wake up at noon. People with the extreme lark mutation wake up at about 4am, but are real party poopers, snoozing at 7pm or so. The whole continuum is believed to be determined by similar small mutations in which just a single DNA base-pair is replaced in one of the clock genes (12 such clock-genes are known so far to operate in mammals).

During a normal night’s sleep, REM occurs every 90 minutes or so. As the night progresses, the REM episodes get longer and the non-Rem periods in-between become shorter (thus still adding up to 90 minutes) as well as shallower. Thus, the really deep sleep (e.g, Stage 3) occurs only during first 1-2 cycles early in the night. Lack of Deep Sleep results in tiredness. Usually adults wake up from REM (children do not), unless waking is forced (e.g., alarm clock). Research on relative roles of REM and NREM in consolidation of memory is very controversial (look for Jerome Siegel on Google Scholar). Growth Hormone surges during episodes of Deep Sleep, and falls during REM, and is almost undetectable during wakefulness.

In the morning, our body prepares us for waking by increasing blood levels of ACTH and cortisol (leading to preponderance of heart attacks at waking time). Our body temperature is the lowest just an hour or two before waking and highest an hour or two before falling asleep. If you feel a chill sometimes when you are up at strange times, it is because your clock is at a pre-waking (late-night) phase.

Melatonin is secreted only at night (circadian clock time) and is not dependent on sleep. However, bright light tends to reduce melatonin levels. In summer, nights are short, thus the duration of the melatonin “signal” is short. In winter, nights are long, thus the duration of the melatonin “signal” is long. The duration of the melatonin signal is the cue that the circadian clock (this is in mammals only) uses to detect season, i.e., the changes in photoperiod (daylength) – information important for timing of seasonal events, e.g., molting, migration, hibernation, reproduction. Humans are only mildly seasonal – our ancestors about 70 million years ago were living in little holes in the ground, were tiny, were nocturnal, were seasonal breeders, and were hibernators. Some traces of our ability to measure photoperiod are retained in “winter blues”, or Seasonal Affective Disorder (SAD). It is almost a form of hibernation.

Phase-disorders of the circadian clock (i.e., extreme larks or owls) can have a similar effect by tricking the melatonin signal (or the reading of the signal by the clock) into believing it is always winter, thus time to be depressed. Lithium treats depression by affecting the period (thus indirectly phase) of the circadian clock (both in vivo and in vitro). In bipolar disorder, manic episodes are characterized by phase-delays and depressive episodes by phase-advances of the diurnal sleep-wake and activity patterns. In a way, phase-delayed people are constantly in the depressive phase of the bipolar disorder.

Treating Extreme Larks and Owls

Trying to regulate sleep-time with melatonin supplements can be tricky. If you are phase-delayed, thus producing melatonin in summer from 2am until 10am, if you take a melatonin pill at 10pm in order to go to sleep earlier, your clock will see a winter-like melatonin signal of 12 hours duration (10pm-10am) and will make you depressed within a couple of days.

The best way to shift a clock is by using bright light. Instead of buying a $500 light-box, you can, for much less money, build your own for a fraction of that money. You need a piece of board, 3-4 strong neon lightbulbs, balasts, a switch, a plug, and some wires. An hour of fun, and you have an apparatus that is just as good and effective as the hifallutin corporate gizmo. Use the light box at appropriate times (dawn for owls, dusk for larks). If you are an extreme owl, when you first get up in the morning, immediately go out in the sunlight (that is thousands of lux of light energy, compared to hundreds from a lightbox) for a jog with your dog. If you do not have a dog, buy one – that will force you to go for a walk early in the morning. Well-scheduled meals also help.

Do not take anti-depressants. They tend to not work for circadian-based depression and may just mask the symptoms (i.e., you “feel” good while your body is falling apart). Do not use melatonin supplements. Do not use alcohol – it may make you fall asleep fast, but the sleep will be shallow and erratic and you will wake up feeling lousy instead of rested. Caffeinated drinks are fine, except during the last 2-3 hours before your intended bedtime, at which time a warm glass of milk may be better.

Make a routine in the evening. The last 2-3 hours before bedtime stay out of the bedroom (bedroom is only for sleep and sex), and switch off all the screens: no TV, no computer, no gameboy. Reading a book while sitting in an armchair in the living room is fine. Just sitting on the porch and thinking will help you wind down. As the evening progresses gradually turn down the lights. Once the bedtime arrives, go to the bedroom, go to bed, switch off the light (pitch darkness) and go to sleep if you can. If you cannot, get up for a few minutes, but keep your lights dim, still no screens, no caffein, no food.

Of course, all of the above are the strategies to shift your clock to a “socially accepted” phase. But you are not crazy or sick. It is the societal pressure to get up at a certain time that is making you sick. Try to get a job that fits your natural schedule. Work at night, sleep during the day (in a pitch-dark, light-tight, sound-proof room) and enjoy life in all its quirkiness.

If you need to go to the bathroom in the evening or during the night, do not turn on the light. Can’t you find your vital organs in the dark? If neccessary, a very dim nightlight (or indirect light from the hall) is OK. If you wake up in the middle of the night, do not get up or switch on the light. Have sex instead. Hopefully your partner will enjoy being woken up by your kinky activities. You will both crash into pleasant deep sleep afterwards. If you do not have a partner, just do it yourself without switching on the lights (as I said, you can find your vital organs in the dark). Jocelyn Elders was onto something….

Why We Sleep Like This?
A classical sociobiological just-so story posits that this kind of individual variation on the lark/owl continuum had an adaptive function, namely to ensure that at every time of night at least one member of the tribe was awake. Thus some stood guard early in the night, others late in the night, listening to the sounds of the jungle (or savannah, or whatever) while the midnight break is thought to have been used for copulating with whomever also happens to be awake at the time – this was before the social invention of sexual monogamy.

Why did cave-men live in caves? Caves are rare and expensive pieces of real estate. If you find one, it is likely to be already inhabited, thus you need to kick out the old tenants (bears?) in order to move in. Then you have to defend it from others who also want this nice piece of property. And it is difficult to defend a cave – it has one entrance – the rest is a trap. If the intruder is really dangerous you have two options: to go out and be killed outside, or remain inside and get killed in the cave. What is so important about the cave that warrants such a risk? Is it that a possible attack can come only from one side, thus requiring only one guard at a time? Is it that newly naked human animals needed shelter from bad weather that they did not need while they were still furry? Is it to protect the newly acquired fire from being extinguished by rain? Does it make easier the task of keeping the herd of not-yet-that-well domesticated animals all together and preventing it from running away? Possibly all of it – we’ll never know – it’s a “just-so” story. But do not forget one very important property of the cave: it is dark inside. It is easy to sleep in the dark. Most animals find shelter or burrow when they want to sleep – this is not just to hide from the enemies and weather, but also to hide from the sunlight.

Sleep is one of the strongest human needs. If you have read the last part of my four-part series featured on the previous Tangled Bank, you have read my ideas why we still don’t know what sleep is for (though see the current state of knowledge in, e.g., this paper: Origin and evolution of sleep: roles of vision and endothermy (pdf)). While I am not advocating ditching modernity, cutting off electricity and going back to the old sleep pattern, we still do not know enough about sleep in order to make the 24-hour society work for us without too much in the way of health consequences.

Hey, teacher, leave us kids alone (to sleep late)

It has been known for a while that adolescents are quite extreme “owls” no matter what their chronotype may be earlier and later in life (and fortunately, school districts are starting to recognize this). This has been attributed to the surge of sex hormones in early adolescence. Responsiveness of the circadian clock to sex hormones has not been studied much (virtually not at all, though I should be able to publish my data within a year or so, sorry for not being able to divulge more detailed information yet), yet most people in the field believe this to be the case, even if no details are available yet.

Now a new paper suggests that the end of adolescence should be defined as a time when the circadian clock goes back to its “normal” state. But, wait a minute, the hormones do not disappear at that time. Thus, if the clock is responding to the hormones at the onset of the adolescence, does this mean that the end of adolescence should be defined as the time when the clock becomes UNRESPONSIVE to the hormones? How does that happen and how is that triggered?

Anyway, I still have to look at the study itself (this is just a press release). I want to see if females both become “owls” AND quit being “owls” earlier than males [OK, I took a peek at the paper and yes, they do]. Also, in women, hormones (mostly estrogen and progesterone) surge in monthly cycles that end abruptly at menopause, while in men testosterone (mainly) is pretty high (with a small circadian variation) continuously and only gradually declines in old age. The lifelong sex difference they found in the study is quite interesting in this light.

Also, I like the way they tried to tease away social influences from pure biology, though they are correct to warn they do not know in which direction causation flows: do the teenagers sleep late because they party, or do they party because they are wide awake…..and now a closet sociobiologist is waking up somewhere in my head trying to explain why would it be adaptive for teens to stay up late and play, including perhaps experimentation with sex while elders are asleep (squash, bad sociobiologist…go back to sleep…there, good boy)….

Wake Me When It’s Over

“Societies define adulthood in different ways, from entering puberty to entering the workforce. But circadian clock researchers now suggest that adolescence ends when we stop sleeping in.Teenagers are more likely to have trouble getting out of bed in the morning than are young children or adults–a finding many studies attribute to a chronic lack of sleep. But researchers at the University of Munich wondered if a more fundamental biological factor played a role.Using a brief questionnaire distributed in clinics, universities and online, Till Roenneberg and colleagues collected data on sleeping patterns from more than 25,000 people in Germany and Switzerland. As part of their analysis, the researchers determined each person’s “chronotype” by calculating the mid-point of their sleep–halfway between going to bed and waking up–on days when the subjects slept as late as they wanted.A surprising pattern emerged. Average chronotypes drift later and laterduring the teen years, but then begin to move steadily earlier after the age of 20, the researchers report in the 28 December issue of Current Biology. It still isn’t clear why, says Roenneberg.

Teenagers may sleep late because they’ve been out partying or they may go out because they’re wide awake at 11 pm. However, he says, the team also saw a similar pattern in teenagers in rural valleys in South Tyrol–where nightclubs are relatively scarce. There, the average chronotype wasabout an hour earlier, but the overall age pattern was the same. The researchers also saw differences between the sexes, with females having an earlier average chronotype than males until around age 50–consistent with menopause–when the correlation between age and chronotype seems to break down. This suggests, Roenneberg says, that biological factors such as hormones have an important influence on the tendency to sleep late.Sleep researcher Mary Carskadon of Brown University in Providence, Rhode Island, says that both social and biological factors are likely involved. Finding the biological trigger–if any–could lead to a better understanding of what drives circadian rhythms, she says.”

Of course, the study was done on Germans. Even in disco-less South Tyrol there is electricity and modernity. It would be cool to see a similar study performed in a culture where sleep is divided in two parts (late-night sleep and afternoon Siesta), like in Mediterranean and Latin American countries, as well as in a real primitive society in which sleep is divided into two parts (early-night sleep and late-night sleep with a break for sex around midnight).

Societal Constraints

One thing we know is that darkness is an important aspect of the environment conducive to sleep. Silence is another. And we do not need science to tell us this – it’s been known forever. I remember, as a kid, learning the “sleep manners”, along with learning how to say “please” and “thank you”, how not to interrupt adults when they were on the phone, and other early lessons of life. By “sleep manners” I mean behavior when there is someone asleep in the house: one is not to enter the room with the sleeping person, not to switch on the lights, not to switch on the noisy appliances (TV, vacuum cleaner, hair dryer or wash machine), not to talk at all if possible, or reduce it to the briefest quietest whisper if absolutely neccessary. One is to walk around on tiptoes, although the best idea is just to leave the house for a while. There was also a ban on telephone use between 10pm and 8am and again between 2pm and 5pm (so-called “house order”). Sleep was treated as something sacred. Be it at night, or the afternoon siesta, only a life-or-death emergency situation warranted waking someone up.

As Robert Anston Heinlein said:

Waking a person unnecessarily should not be considered a capital crime. For a first offense, that is.

One thing I noticed upon arriving to the States is that nobody here seems to have any notion of “sleep manners”. I have seen (and experienced) many times people barging into the room containing a sleeping person, switching on the lights and TV, talking, even talking to the sleeping person, all the while not being even aware that this is a Big No-No, very inconsiderate, and extremely rude. When confronted, the response is usually very defensive, stressing the person’s individual right to do whatever he/she wants and not bother about being considerate about some lazy bum who is sleeping at an inappropriate time. Whoa! Stop right there!

First, individual rights are assumed to mean that you can do whatever you want as long as that does not hurt another person in some way. Waking someone up is harassment – of course it hurts someone. Second, there is no such thing as inappropriate time. If you can, you sleep whenever you can. There is no appropriate or inappropriate time. What do you do if someone is working the night-shift (like my wife often does, and I sometimes do, too)? That person will sleep during the day, so you better shut up. Third, what is this about sleeping being a sign of laziness. The “owls” are constantly being treated as lazy, though they are more likely to be sleep-deprived (cannot fall asleep until the wee hours, then being rudely awoken by the alarm clock after just a couple of hours) and spend more hours awake (and presumably productive) than “larks” do. If you are asleep, this means you need it. If you are rested enough you cannot physically remain asleep or go back to sleep again. You are wide awake. Thus, when you see someone asleep, it is because that person needs sleep right there and then. Sleep is not laziness. Laziness is “lots of front-porch picking”.

Pretending that sleep-need does not exist is also institutionalized. I am not talking just about night-shifts and rotating shifts (those will kill you), night flights, being available for communication 24/7, stores open 24/7, etc – those are part of a modern society, will not go away, and we just need to learn how to adjust. I am talking about the building standards. With a huge proportion of the population working at night, why do windows have no blinds? Some old manors do, but new buildings do not. Never. Some have fake blinds, just for show, screwed into the outside walls on the sides of windows, yet cannot be closed. There are no built-in black curtains, or roll-down wooden blinds. It is difficult to find such curtains in stores if one wants to install one. What is going on? I have never seen, heard, read about, or experienced another country in the world in which sleep is not sacred, and blinds are not an essential part of a house.

I see some striking parallels between the way this society treats sleep and the way it treats sex. Both are sinful activities, associated with one of the Seven Deadly Sins (Sloth and Lust). Both are associated with the most powerful biological needs. Both are supposed to be a taboo topic. Both are supposed to be done in private, at night, with a pretense that it is never actually happening. Education in sleep hygiene and sex hygiene are both slighted, one way or another (the former passively, the latter actively opposed). Both are thought to interfere with one’s productivity – ah, the good old Protestant work ethic! Why are Avarice and Greed not treated the same way? Raking in money by selling mega-burgers is just fine, and a decent topic of conversation, even a point of pride. Why are we still allowing Puritan Calvinist way of thinking, coupled with capitalist creed, to still guide the way we live our lives, or even think about life. Sleeping, whether with someone or alone, is a basic human need, thus a basic human right. Neither really detracts from the workplace productivity – au contraire: well rested and well satisfied people are happy, energetic, enthusiastic and productive. It is sleep repressed people, along with the dour sex repressed people, who are the problem, making everyone nervous. How much longer are we going to hide under the covers?

Perhaps not that long. It appears that we are slowly waking up to sleep problems (pun intended). More and more companies are allowing naps, and even providing nap-rooms. More and more school districts are moving high-school morning schedules later, as during teenage years, under effects of sex hormones, the circadian clocks are all temporarily “owlish”. Adolescents are not crazy and lazy – they physically cannot fall asleep at a normal bed time, and physically cannot awake and feel rested early in the morning (elementary and middle school kids can, as their hormones have not surged yet).

It seems political advisors have caught on, too. During the presidential debates I blogged about the likely tacks used by the handlers to get their candidates to be at their peak performance levels in early evening – something apparently more difficult for Bush than Kerry ( see this and this). Battle for More Free Time, including its subset: the Battle for Sleep, is re-entering the political domain again. Check the links to the websites commenting on this newly-brewing movement. And of course, the art of matchmaking is starting to include the lark/owl questionnaire, assuming that people of the same chronotype are a perfect match (I saw this in a magazine in a waiting room, but if anyone knows if online dating services are doing this, please let me know).

Popping melatonin pills is one of the latest crazes. Melatonin failed as a sleeping pill and its uses as a scavenger of free radicals are dubious at best. It can shift one’s clock, though. However, it cannot help against jet-lag or effects of shift-work (shift-lag) as melatonin is likely to shift only the main brain pacemaker in the suprachiasmatic nuclei. The problem with jet-lag and shift-lag is dissociation of rhythms between cells in different tissues, i.e., your brain clock may resynchornize to the new time-zone/schedule in a couple of days, the clocks in your heart and lungs in a week, and in your stomach and liver in a month. In the meantime, everything in your body is desynchronized and you feel really bad. If you keep changing your work shift over and over again, you never get to achieve complete synchronization, leading to long-term effects on health, including significant rise in heart attacks, stomach ulcers, and breast cancer.

Well, intercontinental flight is here to stay, and some shift-work is neccessary for the modern society to survive. It is now understood that some people (chronotypes) adjust to night-shifts and even properly executed (non-rapid, phase-delaying) rotating shifts, better than others. People have always tried to self-select for various schedules, yet it has recently started to enter the corporate consciousness that forcing employees into unwanted shifts has negative effects on productivity and safety, thus bottom line. See Chernobyl, Bhopal, Exxon Valdese and Three Mile Island accidents – all caused by sober but sleepy people at about 3am, just like thousands of traffic accidents every year.

So how does the future look like? As usual, don’t ask scientists, especially members of the Academy. If you want answers to scientific questions about the future, you have to read science-fiction – this is a sacred duty of all scientists. Cory Doctorow who blogs on the group blog Boing Boing, has written a novel “Eastern Standard Tribe” (you can buy it, or download for free here) that answers just such questions. In the future not so far, people form communities not according to geography, or hobbies, or ideology, but their time zone. Everyone, no matter where on the planet, awake and at the computer at the same time, belongs to a particular Time Zone Tribe. Thus an owl from one country, an average from another and a lark from another will all be typing and reading at the same time, thus will meet in cyberspace and forge alliances against other time-zone communities. Inter-time-zone wars ensue, intrigue and treason happen, boy meets girl…the story is wonderful and will make you think about sleep, and about circadian rhythms, about Internet, and about being human, all in ways you never thought before. Enjoy.

City Of Light: Insomniac Urban Animals

The Cities are the topic of the month here at Scientific American (and at least this week on the blogs), so I should chime in on an aspect of urban ecology that I am comfortable discussing – the effects of increased light at night on animals.

Not all species of animals are negatively affected by the urban environments. Even humans are not driven to insanity by the urban jungle. Some species are really thriving – rats, mice, squirrels, bats, alligators in sewers, sparrows, pigeons, starlings, crows, house flies, mosquitoes and cockroaches come to mind. Many birds have evolved (or invented) quite nifty adaptations to urban life. Of course, animals we domesticated and keep as pets, like cats and dogs, don’t really care about the city vs. country, as long as they are with us and we take good care of them.

But there are definitely negative effects as well. After all, just counts and surveys of species make it obvious that many species are not thriving in dense urban ecosystems. Not all cities are the same either. A large, dense city is likely to be much less hospitable to many species than urban sprawl where much greenery and the original natural habitat are still preserved between the cul-de-sacs. Just watch the wilderness appearing on my back porch: skinks, tree frogs, Luna moths, white-tailed deer, rabbits, opossums, racoons, cicadas, endless species of birds…and I am in the middle of the Triangle, NC.

Large animals, in general, will not do well in cities, and not just because direct encounters with humans can often be deadly (imagine what would happen to a herd of bison if it tried to trek through streets of Manhattan?). Herbivores will be starved due to lack of plants, and carnivores will starve due to lack of herbivores. Thus many ecological factors affect the ability of species to adapt to the City – food, predators, shelter, and, importantly, noise.

But I will focus only on light today. Light pollution is often discussed in the context of impossibility to see the wonderful starry night, but effect of night light on wildlife is a problem beyond human esthetics – it has real-world consequences for the health of ecosystems. And the effect of light almost always involves, in some way, the circadian clock.

Circadian clock – a very, very quick primer

There is quite a lot of biological complexity in the circadian clock, but let’s just remember the few key, basic points.

Circadian clock is a structure (in animals it is in the brain) that governs the daily rhythms of biochemistry, physiology and behavior.

All organisms living on or near the surface of the Earth have a circadian clock. Those that now live deep down inside the soil or rocks or caves, or on the bottom of the ocean, may have secondarily lost the clock that their ancestors once had [1,2].

Having a circadian clock is an adaptation to the cycles of day and night in the environment. Where such cycles are altered, e.g., near the poles, the animals have evolved the ability to turn their daily clocks on or off as appropriate.

Circadian clock keeps ticking in constant darkness, or constant dim light. But in many species, constant intense light disrupts the rhythm.

The clock is reset (entrained, synchronized) each day by the alternation of light and darkness. Species differ as to the intensity of light needed for this resetting to take place. While physiological laboratory experiments usually test the light intensity against the background of complete darkness (in which the sensory systems can get adapted to the dark and become more sensitive to light), it is the difference in light intensity between day and night that is of ecological relevance.

Clock is not a dictator

As much as the circadian clock is “hard-wired” in the brain and determined by the clock-work of genes turning each other on and off, there is still quite a lot of plasticity of behavior – animals can act against the signals from the clock and do stuff at odd times if needed.

For example, when hungry, nocturnal animals will hunt during the day, e.g., man-eating lions hunting at dusk and early night on moon-less night, have to hunt during the day when the moon is full.

Also, these days bats in Austin, TX are flying out earlier at dusk due to prolonged dry weather conditions decimating their food.

Two species of golden spiny mice in Israel live in the same spot – one of them is more aggressive, so the other one has evolved adaptations (including even changes in the eyes) to forage during the day instead of night. Yet, when placed in isolation in the lab, both species are strictly nocturnal, active only at night, which shows that day-time foraging goes against the clock, i.e., is not the adaptation of the clock itself [3].

Finally, when population of rats in a city gets too big, some individuals are displaced. They are displaced in space – foraging on the surface instead of underground – and they are displaced in time – foraging during the day instead of during the night. If you see a rat digging through the garbage bags on the street in the middle of the day, you know that the total population of rats under ground is absolutely enormous! If you are interested in learning more about the fascinating ecology of urban rats, read the wonderful book ‘Rats‘ by Robert Sullivan.

Light at night, clocks and the outside world – behavior

One of the adaptive functions of having a clock is to synchronize one’s activities to that of other players in the ecosystem [4]. You want to go out hunting at the time when your prey is out and about and easy to catch. You want to hide (and sleep) while your predators and enemies are out on the prowl.

But what happens when the difference in the intensity of light is not very different between day and night, as in well illuminated cities? Some species will remain nicely entrained to the cycle, but others will not. Some individuals will be better entrained than others. Some will have their clocks reset over and over again and they will behave at different odd times each day, while in others all rhythms will get lost and they will be out and about all the time.

Thus, many individuals will be going about their lives at inappropriate times, perhaps when the predators are around (and predators are doing the same – one or another will be hunting at any time of day or night), or when the prey is hiding (so too much energy is wasted in looking for elusive food). As a result, many individuals will starve, or get eaten, or miss reproductive opportunities (hey, where are all the potential mates – why are they all hiding and sleeping at the time I am looking for them everywhere?).

Living in an environment in which is is hard to tell if it is day or night is similar to living without having a circadian clock at all. A couple of studies out in the field [5,6,7], with a couple of different species of rodents in which the clocks have been surgically removed from their brains, showed that such animals wonder around at unusual times and are significantly more prone to predation (this is a scientific way of saying: “they got slaughtered by wild cats within hours”).

Light at night, clock and the inside world – physiology

Another adaptive function of the clock is to synchronize events happening inside the bodies, both with each other and with the outside environment. It saves energy if two compatible functions in the body happen simultaneously, while incompatible events are happening at different times. By tuning into the outside cycles of light and dark, the body allocates different biochemical and physiological functions to different times of day, thus saving energy for the animal overall.

And energy is the key. At the time when food is around, it pays to invest energy in finding it. At times when food is hard to find, it is a good idea to use less energy, to stop, hide and sleep. The rate of energy production and use by the body – the metabolism – can be measured in warm-blooded animals (the ‘euthermic’ animals like birds and mammals) by measuring their core body temperature. Higher the metabolism, higher the temperature.

Normally, body temperature cycles throughout the day. Circadian clock drives this cycle so, for example, our bodies are coldest at dawn, and warmest in late afternoon. In birds the difference between the low and high point during the day is routinely a whole degree Celsius. And some small birds, like swifts and hummingbirds, let their temperature drop much, much more during the night (this is called “daily torpor”).

Having or not having food affects how much the body temperature will drop during the night. A hungry animal will save energy by dropping body temperature at night much more than a satiated animal [8]. Yet, temperature will rise to its normal levels the next day in order to give the animal sufficient energy (and speed of reaction) to successfully forage again.

Body temperature drops at night when there is no food, and it also drops during the day if there is no light-dark difference - Ref.8

 

Light affects this: if there is no difference in light intensity between day and night, e.g., in the laboratory in constant darkness, both daytime and nighttime temperatures will fall in hungry animals [8] – they would become too slow and feeble to forage effectively if out in the field. But constant light has the opposite effect – keeping the body temperature artificially high at all times, i.e., not allowing the hungry animal to save energy by dropping its body temperature. The energy balance, especially in a small animal, can quickly become negative, leading to death of starvation.

Reduced perception of day-night changes in light reduces the amount of change and slows down the change in body temperature (top - normal vision, middle - eyeless, bottom - obstructed vision) - Ref.9

 

Light at night, clock and reproduction

In many birds, length of day affects egg-laying in a way that helps the animal determine the total size of the clutch of eggs: how many she lays in one breeding attempt (usually one per year). Data from the laboratory (in chicken, quail and turkeys) [9,10] and from the field (bluebirds [11], also swallows and owls – unpublished data) suggests that this is a widespread mechanism in a variety of bird species.

In early spring, a bird may lay a lot of eggs in a clutch - Ref.10

In late summer, the bird may lay a smaller clutch - Ref.10

If the difference between light intensities at day and night is too small for the bird’s brain to integrate, the bird may be making too much of a breeding effort – laying too many eggs over a period of too many days, perhaps even throughout the year, thus exhausting her internal energy resources, while bringing too many hatchlings to life while unable to feed them all…a disaster all around.

Light at night, clock and calendar

There is a reason for the season. Many organisms do certain things at particular times of the year; breeding, molting, migration and more. The internal “calendar” they use to time such changes in behavior is dependent on the circadian clock which measures the gradually changing length of day throughout the year. The precision of such a measurement can be quite astonishing (see swallows of San Capistrano) [12].

So, what happens if there is not much of a difference between daytime and nighttime illumination? The clock interprets this as constant light, which is the ultimate “long day”, so the animal will constantly be in the “summer mode”, e.g.,. constantly breeding, or constantly trying to migrate or constantly molting its feathers or hair. All of this is energetically costly, and thus maladaptive, and will lead to exhaustion and eventual death of the animal (that is on top of not being in synchrony with other individuals of its species, see above).

Light at night, clock and orientation

When a moth wakes up in the evening and starts flying to find food, it orients by the Moon. It assumes a constant angle to the Moon and keeping that angle allows it to fly in a straight line. After all, the Moon is high and very far away, so flying along does not change the Moon’s relative position in the sky. This is called “transverse” or “Y-axis” orientation.

But the Moon moves across the sky during the night. If a moth is flying for a longer time, it will use its internal clock to compensate for this movement by gradually changing the angle.

What if, instead of the Moon, the moth sees another bright light, perhaps the one on your porch? It starts using it for orientation. At first, it will fly in the straight line. But as it comes closer to the light, the angle changes – the light “moves” in relation to the moth. So the moth compensates by turning in order to keep the constant angle. And then it turns again, and again, and again, spiraling in until it hits the light itself. By that time the light is so close and so bright it looks more like the Sun than the Moon. Its clock gets reset to “day”. So the nocturnal moth alights nearby and, instead of foraging for food, falls asleep. In a wrong place, where it is an easy pick for predators – bats at night, birds at dawn [13,14,15,16].

Birds also orient by celestial bodies. During the day, they orient by the Sun. Again, they use their internal clocks to compensate for the Sun’s movement across the sky. At night, they may use the Moon for orienting, but they certainly use the stars [17]. All the artificial lights become stars. Birds get disoriented, fly in all the wrong directions, and hit the windows and die.

What to do?

This post is really NOT about the solutions, but rather about the underlying science of light effects on animal behavior, physiology and health. I will leave the solutions to others who are experts on engineering or urban policy, who may use the science described above to get informed as to what kinds of solutions may work best.

From what I know, many cities are now starting to tackle the problem of light pollution. Sky lights are banned in some places or at some times of the year (e.g., times of big bird migrations). Many tall corporate buildings now instruct their tenants to turn off the lights at night. There are new designs of street lights that point down – the street below is illuminated even better, much much less light (and diffused, not pointed) goes up to the sky wasting energy and confusing the critters flying by. I am sure there are other things that people do, or things that can be done to reduce the amount of light, or at least the appearance of light sources as “points”, that can be adopted by cities worldwide.

We will never make the cities completely dark at night. And that is OK. After all, the Moon and the stars make nights quite bright out in the wilderness as well. All we need is to make sure that the difference in light intensity between day and night is sufficient for animals to entrain their clocks properly to the daily cycle of bright-light and not-as-bright-light, and they should be fine.

References:

[1] Lee, D.S. (1969). Possible circadian rhythm in the cave salamander Haideotriton wallacei. Bull.Maryland Herp.Soc. 5:85-88.

[2] Trajano, E. and Menna-Barreto, L. (2000). Locomotor activity rhythms in cave catfishes, genus Taunayia, from Eastern Brazil (Teleostei: Siluriformes: Heptapterinae). Biol.Rhythm Res. 31:469-480.

[3] Kronfeld-Schor, N., Dayan, T., Elvert, R., Haim, A., Zisapel, N. and Heldmaier, G. (2001). On the use of time axis for ecological separation: Diel rhythms as an evolutionary constraint. Amer.Nat.158:451-457.

[4] Fleury, F., Allemand, R., Vavre, F., Fouillet, P. and Bouletrau, M. (2000). Adaptive significance of a circadian clock: temporal segregation of activities reduces intrinsic competitive inferiority in Drosophila parasitoids. Proc.R.Soc.Lond.B 267:1005-1010.

[5] DeCoursey, P.J., Krulas, J.R., Mele, G. and Holley, D.C. (1997). Circadian performance of Suprachiasmatic nuclei (SCN)-lesioned antelope ground squirrels in a desert enclosure. Physiol.&Behav. 62:1099-1108.

[6] DeCoursey, P.J. and Krulas J.R. (1998). Behavior of SCN-lesioned chipmunks in natural habitat: a pilot study. J.Biol.Rhythms 13:229-244.

[7] DeCoursey, P.J., Walker, J.K. and Smith, S.A. (2000). A circadian pacemaker in free-living chipmunks: essential for survival? J.Comp.Physiol.A 186:169-180.

[8] Herbert Underwood, Christopher T. Steele and Bora Zivkovic, Effects of Fasting on the Circadian Body Temperature Rhythm of Japanese Quail, Physiology & Behavior, Vol. 66, No. 1, pp. 137-143, 1999

[9] Zivkovic BD, Underwood H, Siopes T., Circadian ovulatory rhythms in Japanese quail: role of ocular and extraocular pacemakers, J Biol Rhythms. 2000 Apr;15(2):172-83.

[10] Zivkovic, B.D., C.T.Steele, H.Underwood and T.Siopes. Critical Photoperiod and Reproduction in Female Japanese Quail: Role of Eyes and Pineal. American Zoologist 2000, 40(6):1273 (abstract).

[11] Caren B. Cooper, Margaret A. Voss, and Bora Zivkovic, Extended Laying Interval of Ultimate Eggs of the Eastern Bluebird, The Condor Nov 2009: Vol. 111, Issue 4, pg(s) 752-755 doi: 10.1525/cond.2009.090061

[12] BD Zivkovic, H Underwood, CT Steele, K Edmonds, Formal Properties of the Circadian and Photoperiodic Systems of Japanese Quail: Phase Response Curve and Effects of T-Cycles, Journal of Biological Rhythms, Vol. 14, No. 5, 378-390 (1999)

[13] Kenneth D. Frank, Impact of Outdoor Lighting on Moths: An Assessment, Journal of the Lepidopterists’ Society 42 (no. 2, 1988): 63-93.

[14] Sotthibandhu, S. & Baker, R.R. (1979). Celestial orientation by the Large Yellow Underwing Moth, Noctua pronuba L. Anim. Behav., 27, 786-800.

[15] Baker, R.R. (1979). Celestial and light trap orientation of moths. Antenna, 3, 44-45.

[16] Baker, R.R. & Sadovy, Y.J. (1978). The distance and nature of the light-trap response of moths. Nature, Lond., 276, 818-821.

[17] Sauer, E.G.F. and E.M.Sauer, 1960. Star Navigation of Nocturnal Migrating Birds. In Cold Spring Harbor Symposia on Quantitative Biology, Vol. 25. pp.463-473.

Images: U.S. light pollution map: NOAA; San Francisco at night, by Thomas Hawk on Flickr (part of the Ligh pollution Flickr collection); Moth attracted by porchlight from Wikimedia Commons. The rest of the images are drawn by me, including from my papers (the original raw files, not copied from final PDFs).

BIO101 – Cell Structure

As you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

Today, we continue into biology proper – the basic structure of a (mainly animal) cell. See the previous lectures:
Biology and the Scientific Method.

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Do you love or hate Cilantro?

This post, originally published on April 25, 2009, although relatively short (for me, at least) and relatively devoid of new information, was a huge hit. It got lots of traffic, many comments, many incoming links, and the discussion spread around online social networks and lasted for quite a while. All it shows, really, is how passionate people are about their food….

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If you think that political or religious debates can get nasty, you haven’t seen anything until you go online and see how much hate exists between people who love cilantro and those who hate cilantro. What horrible words they use to describe each other!!!!

Last weekend, I asked why is this and searched Twitter and FriendFeed for discussions, as well Wikipedia and Google Scholar for information about it.

First – cilantro is the US name for the plant that is called coriander in the rest of the world. In the USA, only the seed is called coriander, and the rest of the plant is cilantro.

Second – there are definitely two populations of people: one (larger) group thinks that it is the best taste ever, while the other group thinks it is awful. The latter group is not simply incapable of tasting cilantro – they can taste it in minuscule quantities hidden in food and describe it as “dirty dish-soap water taste”. People who cannot stand cilantro leaf are perfectly OK with eating the coriander seed.

So, it is something in the leaf that makes the difference.

Third – anecdotal information from scouring the Web suggests (“me and my Dad hate it…”) that the type of response to cilantro is inherited. It is also not experiental (those who hate it, hated it when they were kids, those who love it sometimes first tried it when they were already old and loved it at first try, and the response does not change with age, amount, kind of food preparation, etc).

Fourth – there is no scientific literature that I could find on the genetics of this. Is the difference at the level of the gustatory (or olfactory) receptors, or at higher-level processing centers in the brain?

Fifth – there is one paper that shows that the type of response to cilantro taste has nothing to do with the individual being a supertaster or not.

Sixth – There are a few older papers that identified chemical compounds in the leaves of cilantro, and a few about the allergy to cilantro, but no final identification of the compound that makes the difference in taste to the two groups.

So, does anyone else know more about this? Let us know in the comments.

In the meantime, be nice to people who are not your cilantro-type – they cannot help it.

Image: Wikimedia Commons

BIO101 – Biology and the Scientific Method

Biology and the Scientific MethodAs you may know, I have been teaching BIO101 (and also the BIO102 Lab) to non-traditional students in an adult education program for about twelve years now. Every now and then I muse about it publicly on the blog (see this, this, this, this, this, this and this for a few short posts about various aspects of it – from the use of videos, to the use of a classroom blog, to the importance of Open Access so students can read primary literature). The quality of students in this program has steadily risen over the years, but I am still highly constrained with time: I have eight 4-hour meetings with the students over eight weeks. In this period I have to teach them all of biology they need for their non-science majors, plus leave enough time for each student to give a presentation (on the science of their favourite plant and animal) and for two exams. Thus I have to strip the lectures to the bare bones, and hope that those bare bones are what non-science majors really need to know: concepts rather than factoids, relationship with the rest of their lives rather than relationship with the other sciences. Thus I follow my lectures with videos and classroom discussions, and their homework consists of finding cool biology videos or articles and posting the links on the classroom blog for all to see. A couple of times I used malaria as a thread that connected all the topics – from cell biology to ecology to physiology to evolution. I think that worked well but it is hard to do. They also write a final paper on some aspect of physiology.

Another new development is that the administration has realized that most of the faculty have been with the school for many years. We are experienced, and apparently we know what we are doing. Thus they recently gave us much more freedom to design our own syllabus instead of following a pre-defined one, as long as the ultimate goals of the class remain the same. I am not exactly sure when am I teaching the BIO101 lectures again (late Fall, Spring?) but I want to start rethinking my class early. I am also worried that, since I am not actively doing research in the lab and thus not following the literature as closely, that some of the things I teach are now out-dated. Not that anyone can possibly keep up with all the advances in all the areas of Biology which is so huge, but at least big updates that affect teaching of introductory courses are stuff I need to know.

I need to catch up and upgrade my lecture notes. And what better way than crowdsource! So, over the new few weeks, I will re-post my old lecture notes (note that they are just intros – discussions and videos etc. follow them in the classroom) and will ask you to fact-check me. If I got something wrong or something is out of date, let me know (but don’t push just your own preferred hypothesis if a question is not yet settled – give me the entire controversy explanation instead). If something is glaringly missing, let me know. If something can be said in a nicer language – edit my sentences. If you are aware of cool images, articles, blog-posts, videos, podcasts, visualizations, animations, games, etc. that can be used to explain these basic concepts, let me know. And at the end, once we do this with all the lectures, let’s discuss the overall syllabus – is there a better way to organize all this material for such a fast-paced class.

Today, we start with the very beginning – the introductory lecture on Biology and the Scientific Method. Follow me under the fold:

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Welcome to A Blog Around The Clock – Next Generation.

The day has finally arrived – the new Scientific American blog network is live! And, after almost a year of relative rest, my blog is about to get active again, with substantive posts coming up on a regular basis.

For my old readers who followed me here – you may not be as interested in my introduction below, as it is a partial rewrite and re-edit from several of my old posts, so just pick up the new feed and go check out all the other bloggers on the new network.

But before you leave, you may also be curious to know who made the delightful new banner? It is the artistic creation of Claire Fahrbach, a young artist, illustrator and designer from North Carolina who recently moved to San Francisco in search of a job and a career. See the banner big (and click to see even bigger):

Now for the new readers…a little bit about myself and about this blog. I don’t often write about myself, but every blog needs to have something biographical so readers can figure out where the author is coming from, what to expect, how to connect.

I was born in Belgrade, Yugoslavia (now Serbia). I always loved animals and planned to do something with them, perhaps become a biologist or a veterinarian (or join a circus, or work at a zoo). I grew up in a family that valued language, art, theater, literature and scholarship, so I grew up to be quite a bookworm.

In school, being a brainy math geek and science nerd did not make me ostracized – it made me popular. It was a different time in a different place. It was a different culture. Ever since, I have been trying to re-create that kind of culture around me – make it possible again for a science geek to be seen as cool (for example, getting a picture of myself taken, right, with an inflatable toy sauropod on my shoulder – click to see big).

I was in vet school at the University of Belgrade when the war broke out in 1991. I escaped the country a week before, on one of the last trains out before the borders closed, sanctions were imposed, and the country descended into a decade of chaos. Several flights later, I found myself in North Carolina and, after a couple of years of getting my bearings, decided not to pursue veterinary medicine any more, but to go back to basic science – biology at North Carolina State University.

I did research on circadian (daily) and photoperiodic (seasonal) rhythms in a bird, Japanese quail. I wanted to understand how a brain measures and perceives such long periods of time, and especially how sex hormones affect this timing, which is relevant for understanding why human adolescents cannot fall asleep at night and then wake up in the morning, as well the subtle differences between the sexes (you can click on the image, left, to see large so you can see the quail – orange breasted one is a male, mottled gray-white is a female).

After ten years of grad school, I realized that things I was good at – thinking, connecting ideas from disparate research traditions, designing clever experiments, observing animal behavior, animal surgery, discussing, teaching, placing my work in historical and philosophical context – were going out of fashion. Instead, biology was becoming more and more an exercise in things I was bad at – pipetting all day and running gels, following recipes, doing what I am told to, working at the bench in complete silence for 13 hours a day seven days a week, getting all secretive and competitive.

So I bailed out. While I was still finishing up my last experiments, I started blogging about politics. When the 2004 election was over, I switched to blogging about science and science education. Then I fused those three interests into a single blog. The rest is history.

Now you probably understand the name of the blog and the banner better. The quail on the banner is my old laboratory model animal (Coturnix japonica – I am also known online as ‘Coturnix’). The clock, on the banner and in the title, symbolizes the Biological Clock, the subject of my research. The Web is, of course, the World Wide Web that connects us all. And the blog name as a whole, apart from alluding to my scientific interest, also dates me back to the 1960s (when The Beatles rocked around the clock, with their version of the Bill Haley song), and refers to the question I often get: “Do you ever sleep? You seem to be online around the clock!”.

While much of what I do these days has something to do with writing and publishing and the media, I still find it strange to think of myself as a science journalist. While I still sometimes blog about science, I more often write about meta-stuff, e.g., about science communication, science blogging, science journalism, science publishing, science education, media in general etc. I have not published any articles printed on paper in legacy media and while I am open to that possibility, I am not actively doing anything to make that happen – I feel at home on the Web. I am active on Twitter, Facebook, Tumblr, Posterous and numerous other online spaces. My blogging has brought a number of jobs, gigs and other opportunities.

Together with my friend Anton Zuiker, I organize an annual conference on the intersection between science and the Web – ScienceOnline. The fifth one was a few months ago, and the sixth one will be in January. Every year I also conduct blog interviews with some of the participants of the conference.

Anton and I also teamed up with some friends and built two aggregators you may be interested in – Scienceblogging.org (organized by networks) and ScienceSeeker.org (organized by topics). Both are, we think, useful starting points for exploring and keeping up with the science blogosphere and news.

I also edit an annual anthology of the best writing on science blogs, The Open Laboratory. The next, sixth edition of the book will be published by FSJ/Scientific American.

More recently, I got interested in promoting young and new science writers, and thus in the way science programs work in schools of journalism. I am currently on the advisory board of the Medical and Science Journalism program at UNC, and, starting in September, will be a Visiting Scholar in the Science, Health and Environmental Reporting Program at NYU.

To get a sense of kinds of topics I like to cover, here are some of my most recent posts:

Circadian clock without DNA–History and the power of metaphor

The line between science and journalism is getting blurry….again

Me and the copperheads–or why we still don’t know if snakes secrete melatonin at night

Web breaks echo-chambers, or, ‘Echo-chamber’ is just a derogatory term for ‘community’ – my remarks at #AAASmtg

Cicadas, or how I Am Such A Scientist, or a demonstration of good editing

Giant Dino exhibit at the American Museum of Natural History, or why I should not be a photojournalist

A “sixth sense” for earthquake prediction? Give me a break!

Book review: Pink Boots and the Machete by Mireya Mayor

And if you want more, I have compiled some selections of my best old posts about the media and posts about biology.

A Missing Link Found (and subsequently Lost) at the SciAm Guest Blog

Here is a treat for you at the Scientific American Guest Blog. Today’s contribution is by Brian Switek – check out Breaking Our Link to the March of Progress. Read, enjoy, comment (at the registration the system suggests that you need a confirmation e-mail – you don’t, just log in and start posting).

Guest Blog at Scientific American – second guest post: We all need (a little bit of) sex

As I noted yesterday, the Scientific American Guest Blog is about to get really busy! Already today we have another new post – We all need (a little bit of) sex by Lucas Brouwers (blog, Twitter). Go and check it out and post comments (it takes a second to register).

Written In Stone: interview with Brian Switek

2010 is an incredible year for science books, many written by people who daily write on blogs.

The latest in this fantastic streak is Written In Stone (homepage, IndieBound, Amazon) by Brian Switek (blog, Twitter).

Written In Stone is officially published today. If you pre-ordered it, it should hit your mailbox in a few days and bookstores should get it soon after (watch Brian’s blogs for updates – there was a small delay in shipping). I got the book earlier, have read it and loved it – my review is coming here later today. But first, I wanted to catch up with Brian and ask him a few questions about his book, his blog, and how the two are connected.

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A few years ago, you were a student and blogging was a hobby – something you did on the side, out of love. At what point did you realize that you could do writing as a profession? Was there a precipitating event or did that gradually dawn on you?

There wasn’t any single event or cause – I just fell into it. Now that we’re mostly beyond the blogger vs. journalist sniping – I hope – I can look back and say that I was acting like a science writer even before it became a viable career option. Making the transition required a change in attitude and a realization that I could actually get paid for what I like to do, and I feel exceptionally lucky that I have been able to turn my hobby into a nascent science writing career (even though I still work an unrelated day job to keep the lights on at home).

The more detailed story goes like this – After blogging for two years, I got serious about my science writing and started to pitch to magazines. My performance was abysmal. Most of the time I didn’t even hear back from the publications I pitched to. Still, I kept using my blog as a writing laboratory and tried to fine-tune my writing. Then, in May of last year, everything changed almost instantaneously. It was at that time that I started working with my literary agent – Peter Tallack of the Science Factory – and Mark Henderson of the Times was kind enough to give me my first formal op-ed about the Darwinius controversy. Those breakthroughs, paired with the earlier acceptance of my first academic paper (just published), allowed me to build up enough momentum to start making some headway into more formal channels of science writing outside the blogohedron.

I wouldn’t be able to do what I do without blogs, Twitter, or the web in general. Blogging allowed me to practice writing, plug into a community of fellow science enthusiasts, and has otherwise made it possible for me to become a professional – if still part-time – science writer. If I tried to do the same thing just a few years ago, or otherwise tried to jump into science writing without developing my writing online, I would have almost surely failed. As I mentioned above, though, I did not think of my efforts as a career change. The only major difference was that people started paying me for the sort of work I had been doing anyway!

How did you decide to write a book? You were already a well-known blogger and have started appearing in more mainstream media on occasion – why a book?

Written in Stone had a relatively long gestation and significantly changed since the time that I was first inspired to write a book. I knew that I wanted to write a book about evolution from the time I started blogging, but I was pretty clueless as to how to go about it. I used my blog as a way to practice writing, keep up with the literature, and organize my ideas. Blogging gave me an incentive to keep learning, researching, and sharing that information with whoever cared to read it.

This went on for about three years. I kept notes and wrote parts of a few chapters, but I didn’t have a story to tie things all together. I knew that I wanted to write about evolution from the perspective of the fossil record, but that’s not a book – I needed a more specific angle from which to approach the bigger story of life through time. I knew that I didn’t want to write a comprehensive textbook – we’ve already got plenty of those – but what examples should I choose to help people understand what fossils tell us about how life has changed?

Unfortunately I can’t remember the moment the idea struck me, but I settled on looking at some of the major transitions in the history of vertebrates that transfixed me as a child. The evolution of the first tetrapods from fish, the evolution of birds from dinosaurs, the evolution of whales from terrestrial mammals, the evolution of humans, and others – they were classic examples of evolutionary change, but as I became more familiar with the scientific literature I felt that the public wasn’t being presented with the latest science about these examples. Even in recent popular books about evolution, a few of these transitions would be presented but usually in such paltry detail as to be unconvincing to anyone who didn’t already agree that evolution is a reality. More than that, these changes have been debated for a very long time but we often talk about them only in reference to recent discoveries. I wanted to dig into the long history of debate and show how our understanding has changed. In distilling everything down to simple, step-by-step diagrams of evolutionary change, I felt like other authors had missed something, and I wanted to plug that gap in the popular literature.

Once I figured all that out, writing the book wasn’t too difficult. I had been rummaging through the literature for my own education for several years already – it was mostly a matter of writing the thing. With three chapters in hand, I signed with Bellevue Literary Press in September and completed the first full draft of the manuscript just two days before Christmas. The manuscript went back and forth a few times over the following months for edits, but, looking back, I am still a little baffled as to how I put the whole thing together so quickly!

Your writing – both on the blog and in the book – looks at evolution, focusing mainly on fossils, in the context of history of science. This is a pretty unique combination of themes – where did that come from? Was that a conscious decision or something that just happened as it combined your existing passions?

The mix of evolution, paleontology, and the history of science happened organically. They all overlap and feed into each other. Since I wanted to write about what the fossil record tells us about evolution, those aspects of the story came together very easily. I could have left it at that, but then I would have done the same thing as everyone else by divorcing recent discoveries from their context. I didn’t want to do that. I did not want to act as a figure of authority, handing down data for the public to digest and accept.

Instead of taking the more traditional approach, I wanted to give the book a warmer tone – I wanted to present science in the way that I might talk to a curious friend about evolution, or in terms of what I might say if I were walking with someone through a natural history museum. The history of science allowed me to do this by providing me with a flowing narrative which encompassed the scientific points I wanted to talk about. This served the dual purpose of placing recent discoveries in context and also gave me a way to lead readers through the tangled process of scientific discovery. This was especially important in the historical chapters about the beginnings of paleontology and evolutionary theory (Ch. 2 and 3). I found the idea of simply laying out the nuts and bolts of stratigraphy, natural selection, the nature of the fossil record, etc. repulsive – as I mentioned, I had no intention of writing a textbook – but by tracing the history of science I could use stories to introduce readers to those same concepts in a more palatable way.

Naturally, my own interests played a role, as well. I am fascinated by vertebrate paleontology, and both evolutionary theory and the history of science remain important in the field for understanding the patterns of life on earth and how our perspective of those patterns has changed. It was not a stretch to bring it all together. Paleontology is an evolutionary science, and paleontologists are constantly reexamining old specimens and localities. Given all these available perspectives, it was mostly a matter of choosing where to place the emphasis.

The book grew out of your blog. What proportion of the book, can you estimate, comes directly from edits of your older posts, and how much was brand new material? Was it difficult to repurpose the bloggy format into something that will work well in the book form?

The book grew out of my blog in the sense that I used my blog to practice writing about some studies and ideas which eventually became incorporated into the blog. The book is not just a stitched-together collection of posts. It was written as a story unto itself – containing many smaller stories – and even when I covered something I had blogged about earlier I disregarded what I had already said and wrote something fresh. Sometimes I would dig back into my posts for something I had referenced which I had trouble remembering, but in no instance did I edit any of my posts to place that material in the book. I wanted to write in such a way that the story flowed, and I felt that if I was going to start incorporating material directly plucked from the blog I would jeopardize that. Readers of my blogs will see some familiar subjects, absolutely, but, barring quotations, the book is 100% new writing.

Reading the book, it struck me how unique it is and how much it fills a glaring gap in the literature. There are many books on evolution. There are many books on the history of science. There are many books about fossils (though usually narrower in subject, focusing on a single group like dinosaurs, or even a single fossil like Tiktaalik or Darwinius). Yet I cannot remember another book that combines these three topics until today (literally today!). While it is fortunate for you that this niche was wide open for you to fill, do you have any thoughts as to why this niche was empty to begin with? Aren’t there other scholars who could have, perhaps should have, covered this area in this way?

I think some historians of science have written similar books, but they have usually been focused on a particular time period of group of researchers (such as Adrian Desmond’s Archetypes and Ancestors about Victorian paleontology, Peter Bowler’s Life’s Splendid Drama about early 20th-century paleontology, or Eric Buffetaut’s sadly out-of-print A Short History of Vertebrate Paleontology). When you’re dealing with the history of paleontology, you have to include biological details as well as historical ones, and in many ways this historical subgenre was very influential in determining how I should go about telling my story.

You’re absolutely right about the gap in the literature, though. I intentionally wrote this book to fill it. There’s no single reason why the gap was left open to start with. From a practical perspective, the history of science is often left out of popular books because there is a common assumption that the public doesn’t care about it. One publisher I spoke to about the book early on, in fact, wanted me to cut all the historical material from the book and focus only on new discoveries – from science magazines to book publishers, there is a major push to cover what is new and exciting and leave the historical bits for people who want to track them down (despite the success of some books, such as Bill Bryson’s A Short History of Nearly Everything, which have a heavy emphasis on history!). An exception is Sean B. Carroll’s recent book Remarkable Creatures, but, while I greatly enjoyed it, the treatment of significant people and specimens was a collection of snapshots which did not illustrate the importance of paleontology to our understanding of evolution. There are gaps and jumps in my narrative too – if I included everything I wanted Written in Stone would have rivaled The Structure of Evolutionary Theory in length – but it was very important to me to trace ideas through multiple shifts in understanding over the past 150 years.

The fact that many recent, popular-audience books about evolution – such as Why Evolution is True by Jerry Coyne, The Greatest Show on Earth by Richard Dawkins, and Only a Theory by Kenneth Miller – have been written by lab-based evolutionary scientists is another reason for the persistence of the “paleo gap.” Paleontology isn’t their field and so, understandably, doesn’t get much attention from these authors outside of transitional forms in the fossil record. More than that, though, there is something of a conceit that genetics and microbiology are more important to evolutionary science than paleontology is. Paleontology is still often viewed as the search for old bones to fill museums with – it can demonstrate the reality of evolution by do little else. This appraisal of paleontology has been around since the beginning of the 20th century, at least, and Dawkins even downplayed the importance of the fossil record to understanding evolution in his book The Ancestor’s Tale.

Since Stephen Jay Gould died in 2002, we haven’t really had a strong public advocate for paleontology as an essential evolutionary science. I’m no Gould, but I was inspired by his work to communicate the relevance of the fossil record to understanding of evolution (as well as similar efforts made before him by George Gaylord Simpson). Not only does paleontology provide the essential context to understand why life is as it is now – it is the science which showed us that extinction is real and that life has been changing for vast periods of time – but has become arguably the most interdisciplinary evolutionary science. Paleontologists regularly use ideas and techniques from genetics, molecular biology, embryology, histology, geochemistry, and other sciences in addition to comparative anatomy and geology. Having just attended the 70th annual meeting of the Society of Vertebrate Paleontology just last month, I can tell you that paleontology is an exceptionally vibrant field in which everything from the color of dinosaur feathers to the tempo and mode of evolutionary change are being investigated. This makes the rather brief treatment of paleontology in many recent books on evolution all the more irritating – paleontology, as I know it, is not being reflected in discussions about evolution, and I wanted to write a book to help remedy that.

One thing that struck me as I was reading the book is how well fleshed are the characters in the story, people like Lamarck, Darwin, Owen and Huxley, among others. You present them with a nuance that is rarely seen in usual discourse on the history of evolution. How much did you use biographies of these people, their letters and diaries, in trying to understand them as complex personalities, not just cardboard caricatures that we usually see?

I have to admit that I actually did not get to include the amount of detail I wanted – I mostly restricted biographical sections to the period a given authority was working on a particular problem or idea – but I thought it was essential to provide some background as to who these people were and why they did what they did. In the case of Lamarck, for example, I didn’t know anything about his life outside of his ideas about evolution before writing the book, so I thought including a little more information about him would be a small way of helping his public image since he is so often trotted out to be a contrast to Darwin and nothing else.

The sources I used varied from figure to figure. For Cuvier, I relied on various historical papers and Martin Rudwick’s selected translations of his work in Georges Cuvier, Fossil Bones, and Geological Catastrophes, whereas I used Adrian Desmond’s biography Huxley and the naturalist’s original research papers for sections about the man famously called “Darwin’s Bulldog.” The most difficult challenge was Charles Darwin. So much has been written about him that I could not possibly read it all, so in addition to biographical accounts I used the Darwin Correspondence Project and The Complete Work of Charles Darwin Online to dig into his original writings as much as possible. Of course my account of Darwin’s work is framed in terms of paleontology – I could not comprehensively cover everything he did, especially since he was such a prolific naturalist and correspondent! – but I tried to hit the major points of his career leading up to 1859 without derailing the paleontological thread of the book.

Finally – what’s next? I know you will be busy traveling the country promoting the book, but I am wondering if you already have the ideas for the next book?

I actually don’t have many travel plans. I’ll be giving a few talks in the NY-NJ-PA area, but I don’t have the budget to allow for a full-scale book tour. I am going to focus on doing what I do best – keeping up my blogs and trying to find more stories to tell in more formal science publications and journals. If opportunities to travel and talk about the book pop up, I’ll jump, but I have no idea when or where such opportunities will arise.

If anything, I have too many ideas for future books. Some are just the seeds of future projects which will require significantly more background than I presently have to cultivate, whereas others I am already in the process of starting. Right now I am trying to choose between two different projects – one on the “Dinosaur Enlightenment” which is rapidly changing our understanding of the charismatic creatures, and another on the controversial idea of “Pleistocene Rewilding.” I fully intend on writing both, but which comes first depends on an array of factors from my ability to travel to places relevant to the books to the willingness of publishers to jump at the projects. Beyond those, I have at least three more ideas for long-term book projects on three disparate subjects, so with any luck I will be writing for some time to come!

And, as a closing note, thank you for your help and support, Bora. You have been behind my writing from the very beginning, and it has been a pleasure to talk to you about a book which has grown directly from my work online. Your ongoing encouragement has helped drive me to become a more professional science writer, so I am genuinely thrilled that you enjoyed the book.

Thank you so much for the interview. And let’s hope that book sells very well – it surely deserves it.

Molecular Insights into Classic Examples of Evolution Symposium Live Webcast

This looks awesome! I’ll be at NASW in New Haven CT at the time (I think my session is exactly at this time – bummer!) but if I could I would watch it. If you can, you certainly should watch it:

“Molecular Insights into Classic Examples of Evolution” Symposium to be Webcast Live from NABT Conference in Minneapolis

Are you interested in evolution, but unable to attend this year’s National Association of Biology Teachers (NABT) conference in Minneapolis? Would you and your students like to learn more about how molecular approaches are providing new insights into some of the “classic” examples of evolution you discuss in your class? If so, you will be excited to learn that the annual NABT Evolution Symposium will be accessible via live webcast on Friday, Nov. 5th from 1:00 pm to 5:00 pm, Central time.

Teachers and students are encouraged to tune in to all or part of the free webcast for an opportunity to hear internationally renowned researchers discuss their fascinating, cutting-edge work in molecular evolutionary biology. Classrooms all over the world will even be able to submit their questions online and have the speakers respond in real time!

For more information, including speaker names, talk titles and times, please see https://www.nescent.org/media/NABTSymposium2010.php or contact eog@nescent.org.

To view the live, free webcast, simply go to http://dukeuniversity.acrobat.com/nabt2010 at 11 am Pacific/12 pm Mountain/1 pm Central/2 pm Eastern and log in as a guest. (Note: We suggest you do this in advance to test the connection and make sure you can access the site without problems. When you log in successfully you’ll see a “Congratulations” message. If you have problems, please contact eog@nescent.org.)

See the NESCent site for more information:

This year’s Evolution Symposium features four exciting speakers whose research in molecular evolution is revolutionizing our understanding of familiar and compelling examples of evolution. Learn more about Sean Carroll’s work in Drosophila wing coloration and Hopi Hoekstra’s research into the underlying molecular mechanisms of coat color in beach mice. Butch Brodie will present research on the toxin arms race between newts and garter snakes, and Allen Rodrigo will talk about the practical and research value of studies in viral evolution.

Sigma Xi pizza lunch lecture: Images of Darwin and the Nature of Science

From Sigma Xi:

Join us at noon, Tuesday, Oct. 19 here at Sigma Xi to hear NC State University evolutionary biologist Will Kimler talk about “Images of Darwin and the Nature of Science.” Prof. Kimler researches the history of evolutionary ideas in natural history, ecology, genetics and behavior.

Thanks to a grant from the N.C. Biotechnology Center, American Scientist Pizza Lunch is free and open to science journalists and science communicators of all stripes. Feel free to forward this message to anyone who might want to attend. RSVPs are required (for the slice count) to cclabby@amsci.org

Directions to Sigma Xi, the Scientific Research Society in RTP, are here

BIO101 – Current Biological Diversity

In this lecture, as well as in the previous two, I tackle areas of Biology where I am really weak: origin of life, diversity of life, and taxonomy/systematics. The course is (somewhat intentionally) anthropo- and mammalo-centric, for adult non-science majors, but they do have to give talks about the biology of a plant and an animal later in the course. These are also areas where there has been a lot of change recently (often not yet incorporated into textbooks), and I am unlikely to be up-to-date, so please help me bring these lectures up to standards….

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BIO101 – Evolution of Biological Diversity

In this lecture, as well as in the previous one and the next one, I tackle areas of Biology where I am really weak: origin of life, diversity of life, and taxonomy/systematics. These are also areas where there has been a lot of change recently (often not yet incorporated into textbooks), and I am unlikely to be up-to-date, so please help me bring these lectures up to standards….

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BIO101 – Origin of Biological Diversity

Today, and in the following two lectures, I tackle areas of Biology where I am really weak: origin of life, diversity of life, and taxonomy/systematics. These are also areas where there has been a lot of change recently (often not yet incorporated into textbooks), and I am unlikely to be up-to-date, so please help me bring these lectures up to standards….

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