Lots of good stuff in PLoS Biology this week:
Cognitive Dimensions of Predator Responses to Imperfect Mimicry:
Many palatable animals, for example hoverflies, deter predators by mimicking well-defended insects such as wasps. However, for human observers, these flies often seem to be little better than caricatures of wasps–their visual appearance and behaviour are easily distinguishable from those which they are attempting to mimic. This imperfect mimicry baffles evolutionary biologists, because one might expect natural selection to do a more thorough job. Here we discuss two types of cognitive processes that might explain why distinguishable mimics could enjoy increased protection from predation. Speed-accuracy tradeoffs in predator decision making might give imperfect mimics sufficient time to escape, and predators under time constraint might avoid time-consuming discriminations between well-defended models and inaccurate edible mimics and instead adopt a “safety first” policy of avoiding insects with similar appearance. Categorisation of prey types by predators could mean that wholly dissimilar mimics may be protected, provided they share some common property with noxious prey. If predators use experience with multiple prey types to learn rules rather than just memorising the appearance of individual prey types, it follows that different individual predators should form different categories, each including separate types of novel prey. Experimental studies to test these hypotheses should be straightforward, because we can use the relatively simple signals (e.g., striped patterns) with which prey manipulate predator behaviour as tools for investigating cognitive processes that underlie decision making and object recognition in animals’ daily lives.
The data that would change the course of Jonathan Tilly’s career and cause an uproar in the field of ovarian biology almost never saw the light of day. In Tilly’s cell death lab, postdoctoral fellow Tomoko Kaneko had twice repeated her experiments to kill off mouse egg cells, but something was wrong because the egg cell numbers were still high after treatment with a chemotherapy drug. Kaneko consulted another postdoc in the lab, Josh Johnson, and together they tried to determine if she had made a technical mistake or perhaps switched her control and experimental groups.
“All of us ‘knew’ that egg regeneration couldn’t be occurring,” says Johnson, referring to the long-held view that adult female mammals are born with a fixed pool of oocytes, or egg cells, which gradually declines in number with age. The work appeared to be an anomaly, but Johnson prodded Kaneko to take it to their advisor’s office. That 2002 meeting was the birth of an ongoing controversy that has shaken up the field of reproductive biology, with Tilly’s laboratory publishing data they interpret as evidence of egg regeneration occurring in adult mice.
As a rule, genes and chromosomes come in pairs. Sex chromosomes are an exception to this rule. Males of many species have only one X chromosome, a male-specific Y chromosome, and a set of autosomes (AA). Individuals with two X chromosomes and a set of autosomes (XX;AA) are female. Sex chromosomes were first noticed for this distinct unpaired morphology and are now known to have substantially different gene content . These unusual cases have attracted a great deal of attention over the years, not only because of the role they often play in sex determination, but also as windows into more basic features of genes and gene networks. One such feature is the relationship between gene function and dose. Sex chromosomes allow us to question the importance of having a pair of each gene. With current knowledge of gene regulation, one can make an argument that gene dose should not matter. In textbooks and manuscripts, one often finds figures showing the relationship between genes in a pathway or network, replete with elegant feed-back and feed-forward regulatory interactions, parallel pathways, etc. At the transcript level, it seems logical that any inherent 2-fold quantitative difference due to gene dose should be dwarfed, or even nullified, by the high-magnitude changes resulting from transcriptional regulation by proteins that are arrayed at enhancers or silencers. Basic textbook knowledge of genetics also suggests that dose is not very important. Having a single copy of most genes is not deleterious–there are few dominant alleles due to haploinsufficiency. These observations suggest that genes come in pairs to facilitate reproduction, and perhaps to provide a backup in case of spontaneous mutations occurring during the course of somatic development. It seems likely that the dose of most genes is unimportant because of robustness in gene networks, which buffers against noise and mutation .
Akey decision in the life of an organism is whether to be male or female. In Drosophila, each cell makes this choice independently of its neighbors such that diploid cells with one X chromosome (XY) are male and those with two chromosomes (XX) are female. In classic experiments carried out more than 80 years ago, Calvin Bridges made two important conclusions about how sex is determined in flies [1-3]. He showed that the Y chromosome is not a factor and suggested that sex is determined not simply by counting X chromosomes, but by calculating the ratio of X chromosomes to the number of sets of autosomes (known as the X:A ratio). The concept that sex is determined by a mechanism that evaluates the number of X chromosomes relative to autosomes was invoked to explain the observation that animals with two X chromosomes and three sets of autosomes (XX; AAA) develop as sexual mosaics rather than females. According to this model, animals with the same number of X chromosomes as autosome sets (ratio of 1) are female, animals with half as many X chromosomes as sets of autosomes are male (ratio of 0.5), and those with an intermediate ratio (XX; AAA; ratio of 0.67) are sexual mosaics. With the finding that haploid cells (X; A; ratio of 1) are female [4,5], the idea that sex is determined by the X:A ratio became enshrined in the literature.
Like a camera, the eye projects an image of the world onto our retina. But unlike a camera, the eye continues to execute small, random movements, even when we fix our gaze. Consequently, the projected image jitters over the retina. In a camera, such jitter leads to a blurred image on the film. Interestingly, our visual acuity is many times sharper than expected from the motion blur. Apparently, the brain uses an active process to track the image through its jittering motion across the retina. Here, we propose an algorithm for how this can be accomplished. The algorithm uses realistic spike responses of optic nerve fibers to reconstruct the visual image, and requires no knowledge of the eye movement trajectory. Its performance can account for human visual acuity. Furthermore, we show that this algorithm could be implemented biologically by the neural circuits of primary visual cortex.