Category Archives: Genetics

Did I frame that wrong?

As you know, the last several days saw quite a flurry of blog posts about framing science. I posted my thoughts here and I keep updating my post with links to all the new posts as they show up (except the expected drivel by William Dembski, some minor creaitonists and Lubos Motl). Some of the other bloggers ignored my post, many linked to it without comment, and many linked to it with positive commentary – with two exceptions.
One was Larry Moran (who probably skimmed it quickly, found what he did not like in it with his own frame of mind at the time, and used it as a starting point to make his own point) who does not grok framing, but, as I stated in the initial post as well as in comments elswehere, plays an important role in the ecosystem and is and will remain my daily read because he is a great blogger. His “niche” in the blogosphere is a curmudgeon and that is why we like him, even as each one of us occasionally gets to see his double-barrel shotgun aimed at our own faces. Fine. We are definitely on the same side of the famous M&M debate and we can agree to disagree on framing.
The other one was Michael Tobis who I have not heard of before (have you?). He appears to be a new blogger (so he has an excuse for being a novice) and he is a climate scientist on the right side of the political debate on global warming – his blogroll reveals it. He also gets framing quite well: his next two posts on the topic are good – all linked in my post at the bottom, although he liked learning about the concept of Overton Window from Eli Rabbet and not from me.
I was really taken aback by it and I thought that perhaps the guy is conservative and did not like my treatment of conservatism (although I did warn in a parenthesis somewhere in the post that it was not framed to be liked by them). I still don’t know his political position, but it appears that it was my damning of religion that irked him, although I was careful to damn the Righwing version of religion specifically, with a mild slap on the wrist at the liberal religionists for not stepping up more vocally against the Rightwing version.
Perhaps he was disinclined to listen to someone who proclaims to be an atheist in the “About Me” section. He also did not like the graphic I took from the NCSE article by Eugenie C. Scott (which I first saw in Skeptic magazine) for some reason. Some of the stuff he wrote suggested that he may see the world in a hirerachical manner, as I described in several older posts linked from my framing post.
I blog because I like to make friends and have fun. Some people blog because they like to vent and get in flame-wars. He thought I was the latter kind for some reason unfathomable to me. Anyway, he and I agreed that we should be on the same side (at least on science)and there must have been some deep misunderstanding and we agreed to let my commenters be the judge. So, here is the complete exchange and let us know in the comments what you think:
First, he wrote this in his post:

Also Jim points to Blog around the Clock/Coturnix. I’m not sure whether Jim endorses this article, but I surely don’t. Consider this:

The result of training is that scientists are uniquely trained to be poor communicators of science. Scientists – a tiny percentage of any population – are the only people in the society who even try to think and talk in a value-free way, get insulted when someone suggest they shouldn’t do so, and view other people who can’t do so as intellectually inferior.

I think that captures something interesting. I’m not sure I entirely agree with the substance but it’s an interesting idea.
Unfortunately, it’s stated in such an extreme, overstated and confrontational way as to thoroughly offend both scientists and nonscientists in equal measure. One could hardly come up with a way to frame the opinion that does more damage to discourse.
I thoroughly dislike the rest of the “Clock” article. It gets even worse.
Apparently anyone who doesn’t agree with the author about absolutely everything is an inferior being, who has yet to progress to the level of perfection that the author has attained. Charming.
———–snip——————-
Humorous sarcasm about bloggers you disagree with is one thing. It’s fair game.
Arrogant, humorless contempt for huge swaths of humanity is another. There is hardly a worse example of framing the dialog possible than the toxic sludge of this article.
The amazing thing is that this article claims to offer advice on how scientists should approach public communication. Ironically it violates every bit of good advice it can muster and then some. If you want to know how to communicate in your area of expertise, study this article for form rather than content, and then don’t do that.

How can chastising people for looking down at others be perceived as looking down at others? In the comments, I wrote politely and diplomatically, as I usually do:

In case you missed it, that was self-sarcasm. I am a scientist and I am aware that I have been trained to be a uniquely bad communicator to non-scientists. Four years of blogging are slowly changing that, but I am far from being as good as I could have been have I never got scientific training. Obviously I have a lot to learn, as I was not clear enough for you to understand that the humor/sarcasm was targeted at “me” or at worst “we”, not at “you” or “them”. English is also a foreign language to me, which increases the likelihood of such misunderstandings.

His response:

Fascinating. You absolutely had me fooled. I guess I don’t know to what end you managed it.
I saw another of your postings that seemed to have some of the same characteristics as your self-satire. I am not sure what to think now.
I don’t want to discuss my religious beliefs publicly, but I must say that I am no atheist.
I will therefore explictly state that I don’t accept that atheism is a necessary qualification for scientific work, any more than is any other preconceived notion.
I didn’t find your suggestion to the contrary amusing or ironic, and I don’t see the rest of the “framing” discussion treating it that way. I saw another posting that reinforced my impression that you are not only unalterably hostile to religious thought (which is your right) but that you believe that the scientific culture is necessarily of the same mind (which is arguably not your right at all, and is certainly tactically disastrous in a country where most people take religion seriously).
Perhaps you should clarify on your own site.

Hey, you are free to believe in Unicorns, and you have a right to talk about it in public places, and yes, unfortunately, you have a right to teach your belief to your kids (and thus make them go through the painful process of freeing themselves from shackles of religion when they grow up), but you do not have the right to have your beliefs aired by entities – public or private – that do not want to or constituationally are not allowed to (which was the point of the Blog Against Theocracy week, after all, part of which my post was about), and you have no right not to hear people laugh back at you when you talk publicly about Unicorns.
But my response was much more diplomatic, trying to meet him halfway:

I’ve been clarifying it for years.
I am not hostile to religious people, or to personal beliefs. I am hostile to organized religion and what it does to people’s thought-processes and to the politics of the country (and other countries as well). I am hostile to what organized religion does to science.
A blog post, not being 1000 pages long, cannot contain all the caveats every time – it necessarily has to deal with overgeneralizations and stereotypes which have been clarified, defined and explained in old posts. One tends to write for the regulars, and occasionally a newcomer is baffled, as in joining in a TV series in the middle of its fourth year and not being able to figure out who is who immediatelly.
Write yor perceptions of me in a comment on my blog and see what the regulars say.

He added this to his initial post:

Here is an approximation of the evolutionary ladder as displayed in an image on this article (sorry, I don’t have time to do this up as a fancy graphic)
Coturnix (highest possible form according to Coturnix)
People who agree with Coturnix
Atheists who have some quibbles with Coturnix
Agnostics
Unitarians
Christians (lowest form attained by humans according to Coturnix)
Skunks
Maggots
Lice
Anerobic Bacteria
Notice there is nothing whatsoever about science on this chart. The purpose of public communication of science, it is revealed, is to slyly and secretly move people UP the ladder of development so they are more Coturnix-like.
Maybe all of us in some corner of our minds believe there is some ladder of correctness with our own opinions at the top, and people who thoroughly disagree at the bottom. Grownups tend to know enough to temper this with a tad of humility. On the other hand, publishing your secret arrogance is guaranteed not to win you any friends. Publishing it in an article intended to advise people on public communication is, hmmm, perhaps a tiny bit like shooting yourself in the foot to emphasize your message on firearm safety.

Tell that to Eugenie Scott!
Then, in the comments of my first framing post, he wrote:

I thoroughly disliked this article, taken at face value, and said so here.
Coturnix got wind of this and made what I consider to be an astonishing response, that this article is satire.
Quoth he:

In case you missed it, that was self-sarcasm. … Obviously I have a lot to learn, as I was not clear enough for you to understand that the humor/sarcasm was targeted at “me” or at worst “we”, not at “you” or “them”.

Well it fooled me entirely. Did others read this present article as satirical?
It seems to me consistent with at least one other article on this site.
To be specific I also disliked the cavalier dismissal of the research on the heritability of religiosity. The idea seems to me an entirely sound (in the Popper sense) falsifiable hypothesis, and in studying twins raised apart, investigated using a sound methodology. Coturnix’s response to that also, to me, betrayed both arrogance and a nonrational hostility to religion even as an observable behavioral phenomenon.
Coturnix’s further reply was to advise me to consult with his regular readers on this blog, so I am doing so now.
Did you read this present article as satire? What do you think of the exchange on between me and Coturnix on my linked blog article?

All the twin studies in history are suspect, as they were all done by genetic determinists. And the heritability of religion is much better explained by the effects of the environment: parenting, the social norms of the community, etc.- something that interests me (to see if it can be reversed) so I have studied it for quite aliong time. A couple of papers so far suggesting that adherence to particular religion is written in the DNA are laughable. And tendency towards religosity is an interesting area of research, especially as religiosity means several different things: belief in supernatural, enjoying rituals, fitting into the hierarchy, defining in-group vs. out-group, to name just a few. And there were other red flags in that press release as well. Correlation between church-going and altruism? A positive correlation? Altruism based on fear of punishment is not altruism, and neither is altruism towards one’s in-group members. I touched on the distinction between Internal and External Locus of Moral Authority in my framing post as well. And I wrote about my own personal ‘religious’ history before. But why go on that tangent at all?
My response:

It is interesting that, out of such a long post, you picked that one paragraph to highlight and ignored the rest of the article. This paragraph is a tangential insert, which would be excised out if an editor asked me to shorten the article, for instance, as it is not necessary for the main line of argument.
Also, to be clear, not the entire article is self-sarcasm – this paragraph is. The rest is a serious analysis of framing science (and yes, how it relates to framing politics and religion – as the RightWing political and RightWing religious forces have used framing quite well over the decades). This is one of a few places in the article where I intentionally used different/provocative ‘framing’ to see who will react and how [the use of the term "convert" elsewhere in the text was another example of such a trial balloon, which rasied hackles out of Kate, for instance].
I was very careful in my wording in the article as a whole (as I usually am) to highlight my disagreement with Rightwing religion and Rightwing politics, not with religion per se. I just don’t care for that hypothesis, but I have no problem with liberal variants of religions. It’s a free country – people can believe whatever they want as long as they don’t try to preach/teach others and leave others alone to believe whatever they want.
It is interesting that people – atheists and theists alike – assume that because I am an atheist, I just HAVE to be a rabid proselytizing atheist. Not so. Having the “atheist” descriptor in my “About Me” section is sufficient to raise hackles from the religious and to make atheists certain I am the ally, but the nicest thing is that I do not have to write anti-religious screeds ever! And I don’t. There are more fun things to write about (and blogging to me is about having fun and making friends, not about being a curmudgeon and making enemies).
But I do want to know why people believe what they believe – as a scientific hypothesis – because religious belief when organized into big Religions and coupled with big Politics, affects me and other humans in various ways, often negative ways.
So, you can believe what you want, but I’d like to understand why you do, and if you (not you personally, but “one” – got lost in English language again, sorry) do, how it affects the society.
Since you placed your comment in the thread of that ancient post that nobody reads any more, I’d like to ask your permission to promote it to the top of the page (i.e., to copy and paste it into a brand new post) so my readers can see it and comment on it there. Just say Yes or No either here or on my blog somewhere. Thanks.

Growing up in a non-religious place, the word “convert” first brings to my mind currency conversion, then converting a car so it looses its roof, then changing one’s mind on anything in light of new evidence, and only at the end a religious conversion. But I understand that people who grow up inbued with religion will think of that last meaning first – that was an intended lesson in framing right there.
I want my children to be luckier than that (see this, this, this, this, this and this) and grow up as Natural Atheists, not having to go through the pains of either deciding for themselves after drifting around aimlessly, or going through the “deconversion” process.
He said “Yes”, so now you decide….
Related:
Framing Science – the Dialogue of the Deaf
Framing ‘framing’
Did I frame that wrong?
Framing and Truth
Just a quick update on ‘framing science’
Joshua Bell and Framing Science
Framers are NOT appeasers!
Framing Politics (based on science, of course)
Everybody Must Get Framed

How many things are wrong with this study?

Here, have a go at it. Even better, if you can get the actual paper and dissect it on your blog, let me know so I can link to that. Have fun!
Good Behavior, Religiousness May Be Genetic:

A new study in Journal of Personality shows that selfless and social behavior is not purely a product of environment, specifically religious environment. After studying the behavior of adult twins, researchers found that, while altruistic behavior and religiousness tended to appear together, the correlation was due to both environmental and genetic factors.
According to study author Laura Koenig, the popular idea that religious individuals are more social and giving because of the behavioral mandates set for them is incorrect. “This study shows that religiousness occurs with these behaviors also because there are genes that predispose them to it.”
“There is, of course, no specific gene for religiousness, but individuals do have biological predispositions to behave in certain ways,” says Koenig. “The use of twins in the current study allowed for an investigation of the genetic and environmental influences on this type of behavior.”
This research is another example of the way that genes have an impact on behavior. “Society as a whole assumes that home environments have large impacts on behavior, but studies in behavior genetics are repeatedly showing that our behavior is also influenced by our genes,” says Koenig.

Stem Cell Experiment in The Scientist

On The Scientist website you can find their new experimental feature – an article with questions to the public that will be used in forming the articles for the print version of the magazine next month. Go see Special Feature: Stem cell cloning needs you: In a unique experiment we’re inviting you to participate in a discussion that will help shape our next feature on stem cell research and post comments:

We’re inviting people to give us their thoughts and questions on whether we need to rethink the scientific and ethical approach to stem cell cloning to help shape a feature that we’ll be running in the June issue of the magazine. [...] we’re treating this more as an experiment in user participation, which we’d love to do for more articles in future if people respond to this.

The three main questions are:
Is the nuclear transfer challenge one of understanding or technique?
Is it time to reevaluate the ethics of stem cell cloning?
Does stem cell cloning need new terminology?

So, go there and post comments. So far, there are only 17 comments and the thread has already been hijacked by embryo-worshippers. It would be really nice if people could go there and actually address the issue and try to answer the questions. Adding a comment is easy with no special registration hoops to go through. Hey, if you don’t have time to write multiple long comments, you can always blogwhore: post links to your posts in which you have already answered these quesitons in the past.

Genes, green caterpillars and brown caterpillars

About a year ago, there was a great paper about polyphenism in moth caterpillars.
Now, in the new issue of Seed Magazine, PZ Myers uses that example to teach you all about it. Cool reading on one of my favourite topics (outside clocks, of course).

Aquatic Microbial Diversity

Today is a big day on Plos-Biology for the Oceanic Microbial Diversity Genomics. Last night they published not one, not two, but three big papers chockfull of data.
Accompani\ying them are not one, not two, not three, not even four, but five editorial articles about different aspects of this work.
James has already homed in on one important part of the discovery: the preponderance and diversity of proteorhodopsins – microbial photopigments that are capable of capturing solar energy in a manner different from photosynthesis. As always, light-sensitive molecules are thought to be tightly connected to the evolution of circadian clocks so I expect to see some research on this in the near future.
The biggest challenge of this kind of research is how to take gobs of goo, i.e., the collective DNA from everything collected in the samples, and figure out which sequence belongs to whom. How many microbes have really been captured in the sample? How do those microbes look like? What can we say about their biochemistry, physiology and behavior? What can we say about their ecology and their evolutionary history? What counts as a ‘species’ in the asexual world of microbes?
The methods they use to try to start answering those questions are all genomic – other bloggers may be able to better understand and explain the details which involve various sequence alignments and comparisons to known microbial genomes.
What I’d like to see is a more ecological approach: sampling at different places, at different depths and at different times.
Many aquatic organisms, both unicellular and multicellular, are vertical migrants. They may swim up to the surface during the night and sink down to a greater depth during the day (or vice versa). Sampling at two or more different depths at noon and again at midnight and comparing the sequences can separate the genomes – those sequences that always appear together in the sample will belong to the same organism, those that sequester belong to different organisms.
Likewise, some organisms swim up to the surface only once a month during the full moon. Some never do and are always found only at greater depths. There is likely a seasonal change in the community compposition as well.
Of course, it is expected that different species will be found at different parts of different oceans, in rivers and estuaries, in lakes and streams, which can tell us something about the ecology of the organisms in each of these environments.
Finally, repeated sampling over a number of years at the same place, same depth and same time of day/lunar cycle/year will allow us to track the long terms effects of climate change on the aquatic communities.

DNA can look really pretty…

DNA%20pattern_01.png…when painted base-by-base.

Horse Genome Assembled!

Just got this exciting news by e-mail:

Data on Equine Genome Freely Available to Researchers Worldwide
BETHESDA, Md., Wed., Feb. 7, 2007 – The first draft of the horse genome sequence has been deposited in public databases and is freely available for use by biomedical and veterinary researchers around the globe, leaders of the international Horse Genome Sequencing Project announced today.
The $15 million effort to sequence the approximately 2.7 billion DNA base pairs in the genome of the horse (Equus caballus) was funded by the National Human Genome Research Institute (NHGRI), one of the National Institutes of Health (NIH). A team led by Kerstin Lindblad-Toh, Ph.D., at the Eli and Edythe L. Broad Institute of the Massachusetts Institute of Technology and Harvard University, in Cambridge, Mass., carried out the sequencing and assembly of the horse genome.
Approximately 300,000 Bacterial Artificial Chromosome (BAC) end sequences, which provide continuity when assembling a large genome sequence, were contributed to the horse sequencing project by Ottmar Distl, D.V.M., Ph.D. and Tosso Leeb, Ph.D., from the University of Veterinary Medicine, in Hanover, Germany and Helmut Blöcker, Ph.D., from the Helmholtz Centre for Infection Research in Braunschweig, Germany. Production of the BAC end sequences was funded by the Volkswagen Foundation and the State of Lower Saxony.
Sequencing of the domestic horse genome began in 2006, building upon a 10-year collaborative effort among an international group of scientists to use genomics to address important health issues for equines, known as the Horse Genome Project ( www.uky.edu/Ag/Horsemap/ ). The horse whose DNA was used in the sequencing effort is a Thoroughbred mare named Twilight from Cornell University in Ithaca, N.Y. Researchers obtained the DNA from a small sample of the animal’s blood. To download a high-resolution photo of Twilight, go to http://www.genome.gov/pressDisplay.cfm?photoID=20008.
Twilight is stabled at the McConville Barn, Baker Institute for Animal Health, College of Veterinary Medicine, at Cornell University, with a small herd of horses that have been selected and bred for more than 25 years to study the mechanisms that prevent maternal immunological recognition and destruction of the developing fetus during mammalian pregnancy. The research, conducted by Cornell professor Doug Antczak, V.M.D, Ph.D., and funded by the National Institute of Child Health and Human Development, has implications in reproduction, clinical organ transplantation and immune regulation.
In addition to sequencing the horse genome, researchers produced a map of horse genetic variation using DNA samples from a variety of modern and ancestral breeds, including the Akel Teke, Andalusian, Arabian, Icelandic, Quarter, Standardbred and Thoroughbred. This map, comprised of 1 million signposts of variation called single nucleotide polymorphisms, or SNPs, will provide scientists with a genome-wide view of genetic variability in horses and help them identify the genetic contributions to physical and behavioral differences, as well as to disease susceptibility. There are more than 80 known genetic conditions in horses that are genetically similar to disorders seen in humans, including musculoskeletal, neuromuscular, cardiovascular and respiratory diseases. The SNPs are available at the Broad Institute web site ( www.broad.mit.edu/mammals/horse/snp ) and will be available shortly from NCBI’s Single Nucleotide Polymorphism database, dbSNP ( www.ncbi.nlm.nih.gov/SNP ).
The initial sequencing assembly is based on 6.8-fold coverage of the horse genome, which means, on average, each base pair has been sequenced almost seven times over. Researchers can access the horse genome sequence data through the following public databases: GenBank ( www.ncbi.nih.gov/Genbank ) at NIH’s National Center for Biotechnology Information (NCBI); NCBI’s Map Viewer ( www.ncbi.nlm.nih.gov ); UCSC Genome Browser ( www.genome.gucsc.edu ) at the University of California at Santa Cruz; and the Ensembl Genome Browser ( www.ensembl.org ) at the Wellcome Trust Sanger Institute in Cambridge, England. The data is also available from the Broad Institute Web site ( www.broad.mit.edu/ftp/pub/assemblies/mammals/horse/ ).
Over the next several months, researchers plan to further improve the accuracy of the horse genome sequence and expect to deposit an even higher resolution assembly in public databases. Comparing the horse and human genomes will help medical researchers learn more about the human genome and will also serve as a tool for veterinary researchers to better understand the diseases that affect equines. A publication analyzing the horse genome sequence and its implications for horse population genetics is being planned for the future.
———————–

We can start working equine research now!

Just smelling food will make you live shorter – if you are a fruitfly

Just quickly for now without commentary:
Totally cool paper in the last Science:
S. Libert, J. Zwiener, X. Chu, W. VanVoorhies, G. Roman, and S.D.Pletcher
Regulation of Drosophila lifespan by olfaction and food-derived odors
:

Smell is an ancient sensory system present in organisms from bacteria to humans. In the nematode Caeonorhabditis elegans, gustatory and olfactory neurons regulate aging and longevity. Using the fruit fly, Drosophila melanogaster, we show that exposure to nutrient-derived odorants can modulate lifespan and partially reverse the longevity-extending effects of dietary restriction. Furthermore, mutation of odorant receptor Or83b results in severe olfactory defects, alters adult metabolism, enhances stress resistance, and extends lifespan. Our findings indicate that olfaction affects adult physiology and aging in Drosophila possibly through perceived availability of nutritional resources and that olfactory regulation of lifespan is evolutionarily conserved.

From Nature News:

Eating less can lengthen an animal’s life. But now it seems that — for flies at least — they don’t have to actually cut down on the calories to benefit. Fruitflies can boost their lifespan just by not smelling their food.
The result suggests that flies might use their sense of smell — as well as the actual consumption of food — to help determine how rich their environment is, and how they should go about distributing their energy resources.
From flies and worms to rats and mice, animals fed on restricted diets generally live longer than those given abundant food. No one is sure exactly why this is. One theory is that when times are tough and there is little food about, animals channel more of their resources into maintaining their everyday body function, at the expense of putting energy into reproducing. That can extend lifespan.
Scott Pletcher of the Baylor College of Medicine in Houston, Texas, wanted to find out what governs this decision. Smell, he thought, might be one determinant. “We wanted to see whether we could use odor to trick the flies into thinking the environment was more nutrient-rich than it actually was,” says Pletcher.
Normally, cutting a lab fly’s usual food intake in half lengthens its lifespan by about 20%, from 41 to 50 days. But exposing hungry flies to the scrumptious smell of yeast, a favourite food, took away some of this benefit, the team found. “About one-third of the beneficial effects on lifespan are lost,” says Pletcher.
The yeasty odor had no effect on the lifespan of fully fed flies.

And one of th authors gives additional explanation on the Nature News blog:

We measured the reproduction (fecundity) of OR83b flies and controls. Data is in fig 4a, there is no significant difference, when flies are fully fed. We did not present the data but the quality of eggs (percent that hatches, SL observation) seems to be unaffected. Even if flies would perform worser under stress (lay less eggs under stress for example) it is unlikely to be the cause of longevity, since during the longevity experiment, flies are not stressed in anyway.
It is possibe that the dfference is small, so that we can not detect it, but in this case it is unlikly to be the cause of 56% longevity extension.
Additionally, the work from Tatars lab for at least in some systems, uncoupled reproduction from longevity.

Gene?

In the series of “Basic Concept And Terms” (yup, I know, John is well known for misspelling people’s last names, including mine), several people have already chimed in with their own definitions of the “gene”, demonstrating how unclear this concept is and how much disagreement there is among the practitioners depending on the type of research they are doing (e.g, molecular biology, developmental biology, population genetics, evolution, etc.).
See how the term was defined and explained by PZ, Sandra and Greg so far and you’ll see those differences in emphasis.
Now Larry Moran joins the fray with one post on what a gene is not (though many erroneously cling to this definition) and one post on what a gene is, at least from Larry’s perspective. Good reading altogether.

Cloning Domesticated Animals: Pros and Cons

Food From Cloned Animals Safe? FDA Says Yes, But Asks Suppliers To Hold Off For Now:

The U.S. Food and Drug Administration (FDA) has issued three documents on the safety of animal cloning — a draft risk assessment; a proposed risk management plan; and a draft guidance for industry.
The draft risk assessment finds that meat and milk from clones of adult cattle, pigs and goats, and their offspring, are as safe to eat as food from conventionally bred animals. The assessment was peer-reviewed by a group of independent scientific experts in cloning and animal health. They agreed with the methods FDA used to evaluate the data and the conclusions set out in the document.
—————–
The proposed plan outlines measures that FDA might take to address the risks that cloning poses to animals involved in the cloning process. These risks all have been observed in other assisted reproductive technologies currently in use in common agricultural practices.
——————–
In the draft guidance, FDA does not recommend any special measures relating to human food use of offspring of clones of any species. Because of their cost and rarity, clones will be used as are any other elite breeding stock — to pass on naturally-occurring, desirable traits such as disease resistance and higher quality meat to production herds. Because clones will be used primarily for breeding, almost all of the food that comes from the cloning process is expected to be from sexually-reproduced offspring and descendents of clones, and not the clones themselves.

Jake already wrote what I wanted to write, but here it is in a nutshell:
Meat and Milk safety
Meat is meat. Milk is milk. Beef of any other name is still beef.
Cloned animals are not the same as genetically-modified animals. First, cloned animals are NOT identical to their parents. Second, there is no insertion of non-cow (or non-sheep, non-pig, etc) genes into these animals – no danger of aflatoxin, or peanut genes that can trigger allergies. Every protein in the steak of a cloned cow is still a typical cow protein. If you can normally eat beef, you can also eat cloned beef – there is NO chemical difference.
Ethics
Cloning animals can teach us a lot about genetics and development of animals with, probably, some practical applications down the line. I see no need – and apparently farmers don’t either – for mass production of cloned animals. Only animals targeted to be cloned will be champion breeders. And there is no way that Thorougbred racehorses will ever be cloned – even assisted fertilization (i.e., artificial insemination) is illegal (i.e, the animal will not be included in the Stud Book). So, only a few champion breeders from a couple of species (cows, I guess, perhaps sheep and pigs) will be cloned. This is good – to keep this at a minimum, at least for now – as the process of cloning produces a lot of sickly offspring, which raises ethical questions in itself.
Agricultural practice
We already have a virtual monoculture in both plant and animal production for food. Such lack of genetic variation is troublesome as a new diesase (or global warming) may quickly sweep through our herds and deplete our food supply very fast. Making the gene pool even more homogenous in order to raise the meat/milk productivity of our animals just a little bit does not, in my opinion, warrant a widespread use of cloning of domesticated animals. I’d rather support small farmers who purposefully keep rare, unusual breeds of animals like Old-Type Oldenburg horse, Curly Bashkir pony or Mangalitza pig – breeds that contain genes absent from our current gene pool of mass-produced animals and provide a reservoir of useful traits we may need in the future.
Update: On the other hand, a truly genetically modified animals mey be good: Mad Cow Breakthrough? Genetically Modified Cattle Are Prion Free!

Do We Also Taste Just Like Chicken?

Do We Also Taste Just Like Chicken?Perhaps. But we do other stuff just like chicken (December 09, 2004):

Continue reading

Bioengineering a safer mosquito

Scientists building a better mosquito:

Without mosquitoes, epidemics of dengue fever and malaria could not plague this planet.
The skin-piercing insects infect one person after another while dining on a favorite meal: human blood.
Eliminating the pests appears impossible. But scientists are attempting to re-engineer them so they cannot carry disease. If they manage that, they must create enough mutants to mate with wild insects and one day to outnumber them.
Researchers chasing this dream, including an N.C. State University entomologist, know they may court controversy. Genetically modified crop plants such as soybeans, corn and cotton have become common in the United States, but an altered organism on wings would be a first.
Critics of bio-engineering, especially in Europe, view some genetic alterations as unnatural, even monstrous. People fearful of so-called Frankenfood could sound similar alarms over Frankenbugs.
But with advances in molecular biology and millions of dollars from the Bill & Melinda Gates Foundation, this quest may be within reach. And its promise is huge, the scientists say.

Fred Gould, the NCSU entomologist involved in this project, has started a blog and his lab has started a blog, but there have been no updates in months. Perhaps they will post something after this article came out. Or perhaps they can be prodded to post more by commenting or e-mailing them.
Update: This targeted approach is potentially much better than mass-killing and swamp-draining because the males (only females bite!) and many species of mosquitoes are beneficial ecological actors.

GeneBlogging of the Month

Mendel’s Garden #9: Gene-gle Bells Edition is up on Salamander Candy

Honeybee genome completed!

The honeybee genome project has been finished and a bunch of papers are coming out tomorrow. As soon as they become available online I will comment, at least on the one paper that shows that the molecular machinery of the bee circadian clock is much more similar to the mammalian clock than the fruitfly clock – something that makes me very excited.
In the meantime, you can read more about the bees and their genome on The Loom, The Scientist, Scientific American and EurekAlert.

Morlocks and Eloi, oy vey!

Razib and commenters are commenting on this article which appears to be 19th century SF-fantasy repackaged as “serious science” about the future evolution of the human species. Actually, the article is so silly, Razib does not even want to waste time on it and points out only one of the obvious fallacies of the argument, the one about skin color. On the other hand, Lindsay does a thorough and delightful fisking that you may enjoy!
I don’t even know in which ‘channel’ to put this post. I guess it is “biology” but only nominally… as we do not have a “nonsense and having fun with it” channel here on scienceblogs.
Update: John Wilkins adds his 2 cents – and you should listen to him, speciation is his area of expertise.
Update 2: John Hawks and PZ Myers also chime in.
Update 3: Mouse Trap and Darren Naish have their own takes on the story.

Genetics blogging of the week

Mendel’s Garden #8: Harvest Edition is up on Discoverying Biology in a Digital World.

Perhaps on another planet, it really is like that….

In the light of this years’ Nobel Prizes in Physiology and Chemistry (all RNA all the time), it would be interesting to think how would transcription, translation, gene regulation and replication work if DNA has evolved to be like this!?

New study on evolution of vision

For easy-to-understand quick look at the evolution of vision I have to refer you to these two posts by PZ Myers, this post of mine, and these two posts by Carl Zimmer.
Now, armed with all that knowledge, you will curely appreciate the importance of this new study:
Compound Eyes, Evolutionary Ties:

Biologists at the University of California, San Diego have discovered that the presence of a key protein in the compound eyes of the fruit fly (which glow at center due to a fluorescent protein) allows the formation of distinct light gathering units in each of its 800 unit eyes, an evolutionary change to an “open system” that enabled insects to make significant improvements in visual acuity and angular sensitivity. In contrast, beetles (shown surrounding the fruit fly), bees and many mosquito species have the light-gathering units fused together into a “closed system.”
In a paper published in this week’s early online edition of the journal Nature, the scientists report that one of three proteins needed to form these light gathering units is present in the visual system of fruit flies, house flies and other insects with open eye systems, but conspicuously absent in beetles, bees and other species with closed systems. The researchers showed that the loss of this protein, called “spacemaker,” can convert the eyes of fruitflies–which normally have open eye systems–into a closed one. In contrast, the introduction of spacemaker into eyes with a closed system transformed them into an open one.
Charles Darwin was so enamored by the intricate complexity of the eye that he wondered how it could have evolved. “These results help illustrate the beauty and power of evolution and show how ‘little steps’–like the presence of a single structural protein–can so spectacularly account for major changes in form and function,” said Charles Zuker, a professor of biology and neurosciences at UCSD and a Howard Hughes Medical Institute investigator, who headed the research team.

Nobel Prize for Medicine/Physiology

As you have probably heard already, Andrew Fire and Craig Mello have won the Nobel Prize in Medicine for the discovery of RNA interference.
Jake Young explains what RNAi are and what they do and why is this so revolutionary. Then he explains why those two people got the Nobel for this work instead of some others.
Alex Palazzo (also here), Abel PharmBoy, Carl Zimmer, Nick Anthis and PZ Myers have more and explain it much better than I could ever do. The last time the Nobel was given for work I really understand and like was in 1973 – ah, the good old days when the Nobel did not require molecular biology!
Anyway, this is the first time a Nobel was given for something that was discovered at the time when I was already in the lab and I remember the rumors about it around the molecular labs in the Department. Usually it takes decades for the finding to get a Nobel (and in my field, all the “founders” are dead by now), so this was really fast – indicating how important it is.

Development of Spots on Buterfly Wings

A really cool new study:
DailyScience: How Butterflies Got Their Spots: A ‘Supergene’ Controls Wing Pattern Diversity:

To explore the genetic backgrounds of each of these species, the authors crossed different races of each species and genotyped the offspring in order to identify genes responsible for the color patterns. Thus, they were able to map the color pattern controlling loci in each species: N, Yb, and Sb for H. melpomene; Cr for H. erato; and P for H. numata. Using molecular markers within the pattern encoding genic regions, the authors then found that the loci controlling color pattern variation for each species lie within the same genomic equivalent locations.
This “supergene” region therefore seems to be responsible for producing wing pattern diversity in Heliconius butterflies. Such a locus plays what researchers call a “jack-of-all-trades flexibility” rather than a constraining role. Under natural selection, this region presumably functions as a “developmental switching mechanism” by responding to a wide range of mimetic pressures to produce radially divergent, locally adapted wing patterns.

PLoS-Biology Synopsis: Jack-of-All-Trades “Supergene” Controls Butterfly Wing Pattern Diversity:

Using molecular markers developed in the region of the pattern genes, they found that the three loci controlling color pattern variation for each species inhabit the same genomic location. Indeed, the elements controlling white and yellow pattern variation in H. melpomene (N, Yb, and Sb) and H. erato (Cr) are tightly linked to genetic markers that occupy the same position in both species. Similarly, the locus P, which controls whole-wing variation in H. numata, is also linked to the same series of markers.
These results, Joron et al. conclude, suggest that a single conserved locus is responsible for producing wing pattern diversity in Heliconius butterflies. Rather than a constraining role, this locus provides what the researchers call a “jack-of-all-trades flexibility.” It presumably functions as a “developmental switching mechanism” for natural selection, they explain, by responding to a wide range of mimetic pressures to produce radically divergent, locally adapted wing patterns. Now researchers can begin to identify and determine the modus operandi of the genes at the center of what has been called a “developmental hotspot” to better understand how they drive the adaptive evolution of mimetic color pattern shifts.

The PDF of the paper is here.

That Fruitfly Will Beat You Up

Fruit Fly Aggression Studies Have Relevance To Humans, Animals:

Researchers in the North Carolina Sate University genetics department have identified a suite of genes that affect aggression in the fruit fly Drosophila melanogaster, pointing to new mechanisms that could contribute to abnormal aggression in humans and other animals.
The study, led by doctoral student Alexis Edwards in the laboratory of Dr. Trudy Mackay, William Neal Reynolds Professor of Genetics, appears online in PloS Genetics.
Feisty flies themselves may not be very scary, but their genes and biochemistry have more in common with those of humans than the casual observer might suspect, and geneticists can subject flies to experiments that simply can’t be done on higher organisms.
To measure aggression, the researchers starved male flies for an hour and a half, then gave them a small food droplet and watched them duke it out, counting the number of times a focal fly would chase, kick, box, or flick his wings at other flies.
“Some animals will very vigorously defend their little food patch, whereas others are relatively polite,” Mackay said. “To determine if this had a genetic basis, we conducted a selection experiment.”
For the selection experiment, Edwards pulled three groups of flies – high aggression, low aggression and control – from the same baseline population, and kept them separate for 28 generations. From each generation, she selected the most aggressive flies from the high aggression group, the least aggressive flies from the low aggression group, and a random sample of the control flies, to be the parents of the next generation.
All the flies started at the same level of aggression, but after 28 generations of selection, the high aggression groups were kicking, chasing and boxing more often, while low aggression groups would hardly fight at all.

Hey, these are my neighbors from upstairs. And note how Trudy Mackay knows what to tell the reporter so not to end up with one of those “Gene for X” titles:

Selection experiments only show these kinds of results when there is some genetic control over the trait being selected. In this case, the genetic effect was not very strong – the heritability, or genetic contribution to, aggressive behavior was about 10 percent. The other 90 percent had to be attributed to environmental variation.
“This is definitely not genetic predeterminism,” Mackay said. “It’s a susceptibility. Even in flies, in the constant environment in which we grow them, the environment is more important than the genes. But we are very interested in that small genetic contribution.”

Read the rest, it’s cool…

Francis Collins is in town

A Community Genetics Forum 2006: Finding the Genome is a 3-day conference here in the Triangle. I will try to go to the third day events on Saturday, 10am – 3pm.
It is a very medically oriented meeting, so I doubt they will mention the importance of comparative genomics in the study of evolution, but it will be fun anyway.
On the other hand, it is probably good for my emotional well-being that there is likely to be no mention of Francis’ awful book

ERVs in sheep, though essential, do not make them smart

Remember this post from a couple of weeks ago? It was quite popular on tagging sites like Digg, Reddit and Stumbleupon. It was about endogenous retroviruses and their role in the evolution of placenta (which made the evolution of other mammalian traits possible).
Now, there is a new study in sheep, on this same topic, and it looks very good at first glance:
Researchers Discover That Sheep Need Retroviruses For Reproduction:

A team of scientists from Texas A&M University and The University of Glasgow Veterinary School in Scotland has discovered that naturally occurring endogenous retroviruses are required for pregnancy in sheep.
In particular, a class of endogenous retroviruses, known as endogenous retroviruses related to Jaagsiekte sheep retrovirus or enJSRVs, are critical during the early phase of pregnancy when the placenta begins to develop.
—————snip—————-
The idea that endogenous retroviruses are important for reproduction in mammals has been around for about 30 years, Spencer said. Studies in cultured cells have shown that a protein of a human endogenous retrovirus might have a role in development of the human placenta.
The team blocked expression of the envelope of the enJSRVs using morpholino antisense oligonucleotides, which inhibit translation of specific messenger RNA. When production of the envelope protein was blocked in the early placenta, the growth of the placenta was reduced and a certain cell type, termed giant binucleate cells, did not develop.
The result was that embryos could not implant and the sheep miscarried, Spencer said.

Genetics carnival

Mendel’s Garden #5 is up on Evolgen.

My hair-stylist had to buy sheep-shearing clippers for me

Now, this is the gene that was meant to be named “hairy” instead of this one:
Hirsute-s You, Sir! Could Super Furry Animals Provide Clues For Baldness?:

The team found that cells given the genetic command to become hair follicles will send out signals to neighbouring cells to prevent them from doing likewise, so producing a specific hair pattern.
They also demonstrated that by hyperactivating the ‘hair protein’ in embryonic mice, young with considerably more fur than normal were produced.

Did A Virus Make You Smart?

Did A Virus Make You Smart?Not really a review of Greg Bear’s “Darwin’s Radio” and “Darwin’s Children” but musing (practically SF itself) on the topic of these books (from April 20, 2005):

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Books: “Coming To Life” by Christiane Nusslein-Volhard

Several ScienceBloggers are reviewing Coming To Life today (see reviews by Janet, Shelley, RPM, Nick and PZ Edit: Razib has also posted his take), each one of us from a different perspective and looking from a different angle, so go read them to get the full scoop.
PZ Myers reviewed the book a few weeks ago. Someting that struck me was that PZ said that the book :

“….assumes nothing more than that the reader is intelligent and curious. Seriously, you don’t need a biology degree to read it!”

…while a reviewer, Edward F. Strasser (a math PhD whose hobby is reviewing books from this angle – how readable they are for laypeople) on Amazon.com states the opposite:

“I don’t think that a person who has never seen this material before is ready for this book, but I think that many people who need it for review will be OK.”

So, when I started reading the book I decided to try to empty my mind of all the knowledge I have and to read it like a complete lay-person. I wanted to see who is right – PZ or Strasser – and try to determine who is the real audience for the book.
First, I have to tell you that I absolutely LOVED the book. And that may be its biggest problem. The book will be appreciated the best by people like me – biologists with expertise in another field who want to brush up on their evo-devo (and just devo) and have an easy reference on the bookshelf. The book does absolutely great for people like that.
But, will it do the same for others? Developmental biologists do not have a need for it because they already know everything in it and 100 times more. But how about complete laymen, people with minimal formal science education but a keen interest in science, people who read popular science magazines, watch Discovery channel and read ScienceBlogs?
I’d say Yes, but very cautiously. In a way, the book is deceptive. Its small size and pretty cover art suggest a breezy read. But it is not. It is a textbook disguised as a non-fiction bestseller. The tone is a matter-of-fact, unexcited monotone. Trying to speed though it will be a disaster. Why?
A textbook on developmental biology would be an expensive, 1000-page, lushly illustrated avalanche of nitty-gritty details. Making the book small by eliminating a lot of that detail means that what remains is highly concentrated. Every sentence matters. Every sentence is a summary of a thousand papers.
There is no “filler” material, e.g., anecdotes and personal stories or interesting examples of, for instance, exceptions to the the rules in a strange species, or philosophical musings, kind of stuff that will let your focus wane every now and then without serious consequences to understanding. Only occasionally she slides in a little bit of history which is always a welcome change of pace on top of being very informative and placing the material in a historical context.
You need to slow down and read every sentence with concentration. Perhaps stop and think what it means every now and then. Sometimes you wish she has NOT omitted some of the details which may serve as a useful illustration of a big principle she is describing in that sentence or paragraph.
Several times I caught her using a technical word without explaining (or at least defining) it first. If you did not have Intro Bio recently, or are not generally well informed on basic genetics and molecular biology, that would throw you off, and make you rush to the back of the book to check the Glossary – something that breaks the flow of reading any book.
So, the book is great for people who have some biology background (at any level) but not much knowledge of developmental biology – people like sophomore biology majors. But how do you get them to slow down and read the book carefully? Well, use it as a textbook! For an Introduction to Development course. I am serious! It’s that good.
The instructor could spend time in class explaining the principles described in the book – a process which slows down the reading of the book. Then, each instructor is free to add as much or as little detail in lectures as the level of the course requires, plus cool examples, flashy images and videos, etc, and add a couple of more readings, e.g., scientific papers and reviews.
Heck, it could be used even for a General Biology class for science majors (e.g., a summer speed class). Genetics, development and evolution are the core of biology, so adding a couple of lectures (with additional notes or a similar book) on physiology, behavior and ecology at the end (and those can be built upon the edifice of genetics, development and evolution covered before), would work just fine in some contexts, eliminating the need for students (like mine, the adults) to buy huge expensive textbooks that only intimidate them with the wealth of detail. It would give the instructor more freedom to design a course well.
Why do I think that this book is better as a potential textbook than the usual texts? Apart from size, price, friendliness and giving the instructor greater freedom, I really like the way the material is explained.
From the very first sentence, and reinforced throughout the book, the message is that the cell is the smallest unit of life. Not genes. Cells. While most textbooks fall into the philosophically untenable habit-of-mind that “genes use cells to make more genes” or “cells are places where genes perform the work of life”, Nusslein-Volhard constantly explains stuff within the proper way of thinking – “genes are tools that cells use to change, to do their job within the organism, and to make more cells”. The shift is subtle. She rarely states it this directly and openly, but if you are reading the book specifically looking for it (as I did), you notice that the word-choice and the way of explainig things is always within this mode of thought. She also, whenever that is appropriate, never forgets to mention important influences of the internal and/or external environment on cells and tfe developing organisms.
The book also makes a gradual progression over levels. After basic introductions to evolution, heredity and molecular biology, she starts with the cell and how it uses genes to change its own and neighboring cells’ properties. As the chapters move on, there is less and less talk of genes and more and more talk of cells, tissues organs and whole organisms, ending with the return to evolution in an excellent chapter on Body Plans.
Understanding that most of the readers will be anthropocentric, she then devotes a chapter to the development and reproduction in those lousy lab animal models – humans.
The final chapter on controversial aspects of developmental biology and its practice – covering stuff like cloning, stem-cell research etc., is as calm and even-tempered (almost dry) as the rest of the book. More importantly, the conclusions given there are derived directly from the science described in the rest of the book, with no Culture-Wars code-words that can trigger automatical resentment on the part of readers that are involved in Culture Wars on one side or the other. Again, it provides the neccessary background that can be useful for a class discussion. And its dry, science-y tone is exactly what is needed for such a discussion.
So, if you are a biologist and you want to refresh and update your knowledge of development really fast and easy – get this book, it is better than any other in this respect.
If you are not a biologist, but have a keen interest and some background, get the book but do not expect to breeze through it in two hours. Do not be deceived by the small size and pretty illustrations Dr.Volhart drew herself. Give yourself a week to read this book, then read it slowly and with full concentration. Read that way, it is worth its weight in gold.
And if you are more interested in the “evo” side of evo-devo and a more future-oriented book (Coming To Life summarizes current knowledge with no speculations about the future), read “Biased Embryos and Evolution” (see my review) – the two books nicely complement each other.
My question to Dr.Nusslein-Volhard: Is it possible to turn Developmental Systems Theory into a useful experimental program and, if so, will that provide discoveries and insights that are lacking within the current paradigm?

A long stroll through the geneticist’s garden

Mendel’s Garden #4 is up on The Innoculated Mind

Bring back the mammoth, or, not so fast!

Archy is on top of the story, as usual when the story is about people trying to resurrect mammoths!

Zebrafish Rules!

I hope PZ will comment on this study:

A humble aquarium fish may be the key to finding therapies capable of preventing the structural birth defects that account for one out of three infant deaths in the United States today.That is one of the implications of a new study published online August 8 in the journal Cell Metabolism. The paper describes a number of striking parallels between a rare but fatal human birth defect called Menkes disease and a lethal mutation in a small tropical fish called the zebrafish that has become an important animal model for studying early development.
————snip—————
In the paper, the researchers describe the discovery of a mutation in the zebrafish that disrupts the distribution of the critical nutrient copper within the fish cells and causes defects that are remarkably similar to those observed in children suffering from Menkes kinky hair disease, which, in its most severe form, causes degeneration and death within two to three years after birth.
“We found this mutation about two and a half years ago,” said Solnica-Krezel. “Because it impairs so many aspects of normal development and causes the embryo to fall apart in two days, we named it ‘Calamity.'” Six months later, she heard a talk that Gitlin gave at a scientific meeting about the results of exposing zebrafish embryos to a chemical agent that disrupts copper metabolism. She was struck by the similarity between his results and those produced by Calamity, so she approached him and they decided to collaborate.

Clock Genetics – A Short History

Clock Genetics - A Short HistoryA short post from April 17, 2005 that is a good starting reference for more detailed posts covering recent research in clock genetics (click on spider-clock icon to see the original).

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Bioinformatics and Computational Biology

Bio::Blogs #2 is up on Neil Saunder’s blog.

Mendel’s Garden #3

Mendel’s Garden, the carnival of genetics, is up on Viva La Evolucion.

Hot Peppers

I had lunch with Anton yesterday. We talked about the upcoming busy blogging Fall and he showed me his new book.
We ate in my neck of the woods, at Town Hall Grill in Southern Village in Chapel Hill. Anton brought his laptop – the wi-fi signal is strong, so, after Brian and Ruby get married tomorrow (OK, they already are), Brian can add this restaurant to the Chapel Hill Wireless map.
Being very hungry, and knowing that the food there is delicious, I came prepared. While Anton had their lightly-battered fish and chips, I ordered a NY strip.
When the food arrived I reached down into my pocket. Out of the pocket I took out a little bag. Out of the bag I pulled out a hot pepper. Anton was quite amused.
I learned that trick from an old childhood friend of my father. He always had a a couple of hot peppers in his shirt pocket, usually wrapped in a paper napkin and he would eat them with a meal wherever he may be. He even brought them and ate them at dinners at our house although he knew that we would most definitely have some really good and really hot peppers at home – we always did.
hot_pepper.jpg
I grew up loving hot peppers – it was hard not to in my father’s home. It is an acquired taste, I understand. I try to always have one or two at home, but it’s not easy to find really good ones, or at least peppers that remind me of home.
This particular pepper that I had for lunch yesterday I bought at the Southern Village farmer’s market last week. It was delicious! It was not just fantastically hot, but it also had a rich taste and smell of a pepper. I ate less than half of it but enjoyed every nibble.
Later in the afternoon I went to the farmer’s market and told he guy who sold me the pepper how good it was and that, once I manage to eat it all by next Thursday, I’ll be back for another one. He appreciated that.
And all this thinking abot hot peppers made me think about two Big Questions: Why are peppers hot? and Why we like to eat hot peppers? Those evolutionary questions sound like perfect topics for my next two blog posts, coming to your computer monitors soon.

Deceptive Metaphor of the Biological Clock

Sometimes a metaphor used in science is useful for research but not so useful when it comes to popular perceptions. And sometimes even scientists come under the spell of the metaphor. One of those unfortunate two-faced metaphors is the metaphor of the Biological Clock.
First of all, there are at least three common meanings of the term – it is used to describe circadian rhythms, to describe the rate of sequence change in the DNA over geological time, and to describe the reaching of a certain age at which human fertility drops off (“my clock is ticking”).
I prefer the Rube-Goldberg Machine metaphor for the mechanism underlying circadian rhythms, but apparently more people know what a clock is than what a Rube-Goldberg Machine is so it appears that we are stuck with the Clock Metaphor for a while.
Once you have a clock metaphor, it is easy to see a clock everywhere you look. Like seeing nails with a hammer in your hand, a researcher in choronobiology is likely to see timing everywhere – I know, I do it myself.
And sometimes this approach pays off – there is definitely a link between circadian and developmental timing in Nematodes, between circadian timing and timing of the love-song in Drosophila, between circadian and seasonal timing, to name some of the few well-known connections, each discovered by a circadian biologist intirgued by the possibility that a clock at one domain (days) may also be involved in timing at other domains (miliseconds, hours, weeks or years).
One of the most touted, yet the most tenuos connection is that between circadian timing and timing of aging and death. Much funding has already been poured into studying this, but, apart from figuring out how circadian rhythms themselves change with age (yup, like everything else, the clock gets a little sloppy and the rhythms get fragmented so you tend to nap more often), no such link has been found yet.
But funding needs to be renewed, and it is just so easy to mix metaphors here – “my clock is ticking” and “my circadian clock is ticking” are so easy to sell together as a package.
Thus, I was not too impressed when I saw this press release: Link Between The Circadian Clock And Aging:

Studying a strain of transgenic mice lacking the core circadian clock gene, Bmal1, Dr. Antoch and colleagues determined that BMAL1 also plays an important role in aging. Bmal1-deficient mice display a marked premature aging phenotype: By 4-7 months of age, the Bmal1 knockout mice experience weight loss, organ shrinkage, skin and hair weakening, cataracts, cornea inflammation and premature death.
The researchers went on to show that BMAL1’s influence on the aging process is due to its previously established role in protecting the organism from the genotoxic stress. Some BMAL1-deficient tissues – like the kidney, heart and spleen – accumulate aberrantly high levels of free radicals. The scientists believe that oxidative stress may underlie premature aging in these animals.
Future research will be aimed at delineating BMAL1 target genes involved in the aging process, with the ultimate goal of elucidating molecular targets for the rational design of drugs aimed at alleviating specific, age-related pathologies. “The involvement of BMAL1, the key component of the molecular clock, in control of aging, provides a novel link between the circadian system, environment and disease and makes circadian proteins potential drug targets,” explains Dr. Antoch.

If you knock out a gene or two, you get messed-up animals. Genes do not work in isolation – they are parts of multiple networks. Knocking one out will mess up multiplenetworks of genes, thus multiple processed in cells. Cells will then compensate fine-tuning other processes, etc. In short = knockout animals are sick animals.
I was going to completely ignore this, but then I saw this nice put down: Surprisingly Few Processes Can Be Thrown Into Reverse:

You should also bear in mind that the appearance of accelerated aging is by no means an indicator that accelerated aging is in fact taking place. It was something of a big deal that certain human accelerated aging conditions were shown to actually be accelerated aging, for example. As another example, diabetes looks a lot like faster aging in many respects, but it isn’t. Surprisingly few biochemical processes are open to this sort of “let’s find out how to throw it into reverse” logic, but the funding game requires one to pitch the next proposal ahead of time and on the basis of your latest research.

Exactly. Read the whole thing and do not buy stock in synthetic BMAL just yet….

What color were the mammoths?

IceAge2-1.jpg
Archy has the answer.

Tau Mutation in Context

Blogging on Peer-Reviewed Research

hamster.jpgI got several e-mails yesterday about a new study about the molecular mechanism underlying circadian rhythms in mammals (“You gotta blog about this!”), so, thanks to Abel, I got the paper (PDF), printed it out, and, after coming back from the pool, sat down on the porch to read it.
After reading the press releases, I was in a mind-frame of a movie reviewer, looking for holes and weaknesses so I could pounce on it and write a highly critical post, but, even after a whole hour of careful reading of seven pages, I did not find anything deeply disturbing about the paper. Actually, more I read it more I liked it, my mood mellowed, and I am now ready for a long rambling post about it – I have no idea how is it going to end, but let’s go on a journey together….and let me start with a little background – the Big-Picture-kind of background – before I focus on the paper itself.

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JETLAG – new circadian gene in Drosophila

Blogging on Peer-Reviewed Research

drosophila.jpg
In the beginning, there was period.
Before 1995, the only known circadian clock genes were period (Per) in Drosophila melanogaster (wine fly) and frequency (Frq) in Neurospora crassa (bread mold). Some mutations, though not characterized at the molecular level, were also known in Chlamydomonas, Euglena as well as the famous Tau-mutation in hamsters.
I still remember the strained mathematical models attempting to account for a 24-hour rhythm with just a single gene controlling its own expression. We now know that multiple genes are involved in circadian function in invertebrates and vertebrates, many of which are the same across the animal kingdom and even play the same roles within the circadian mechanism.
But back in 1995, the discovery of TIMELESS (tim) by Amita Seghal was a really big deal – here was a protein that binds to Per in the cytoplasm and is degraded by exposure of the animal to light. That was the beginning of the molecular revolution in chronobiology – finally there was a system in which both the freerunning rhythms and entrainment by light could be studied at the level of the molecules.
It is not surprising that Dr.Seghal, among other things, still pursues the study of TIMELESS. Although this gene is not at all involved in the circadian clock in mammals (where the role is taken by cryptochrome, which has its own role in the Drosophila clock), it is one of the key players in the Drosophila system which, in turn, is the key system for every genetic investigation imaginable. In other words, even if the identities of players are different between invertebrates and vertebrates, the logic of the circadian system is likely to be the same.
Drosophila%20clock.jpeg
In the latest paper in Science, Dr.Seghal and collaborators report the identification of a new gene involved in circadian regulation. They named it JETLAG (Jet). In a series of elegant experiments they show that light, by induction of 3D transformation of CRY (cryptochrome protein), induces the phosphorilation of TIMELESS. JET, then, is capable of binding to TIM and helps degrade TIMELESS protein:

Our results, together with those of previous studies, suggest the following model of how light resets the clock in Drosophila. Upon light exposure, CRY undergoes conformational change, allowing it to bind TIM. TIM is then modified by phosphorylation, which allows JET to target TIM for ubiquitination and rapid degradation by the proteasome pathway.

A New Carnival!

Pedro Beltrao, who blogs on Public Rambling is starting Bio::Blogs, a carnival of bioinformatics and computational biology.

Pediatric Garden

The very first edition of Mendel’s Garden, the carnival of genetics, is up on The Force That Through….
Pediatric Grand Rounds, Volume 1 Edition 5, is up on Unintelligent Design.