Sunday, August 17, 2008
In many vertebrates, there is an association between pigmentation and behavior. One potential reason for this is that genes influencing pigmentation also have pleiotropic effects on other traits, including behavior. A recent paper in Trends in Ecology and Evolution lays out this hypothesis:
In vertebrates, melanin-based coloration is often associated with variation in physiological and behavioural traits. We propose that this association stems from pleiotropic effects of the genes regulating the synthesis of brown to black eumelanin. The most important regulators are the melanocortin 1 receptor and its ligands, the melanocortin agonists and the agouti-signalling protein antagonist. On the basis of the physiological and behavioural functions of the melanocortins, we predict five categories of traits correlated with melanin-based coloration. A review of the literature indeed reveals that, as predicted, darker wild vertebrates are more aggressive, sexually active and resistant to stress than lighter individuals. Pleiotropic effects of the melanocortins might thus account for the widespread covariance between melanin-based coloration and other phenotypic traits in vertebrates.
This is clearly far from gospel truth; the authors are laying out the plausibility of this hypothesis and a framework for further exploration. The hypothesis is that higher levels of the molecules that bind the melanocortin receptors (the melanocortins and agouti proteins) lead to both darker pigmentation as well as pleiotropic effects in other tissues (I've mentioned before some of the effects of messing with these receptors in sexual behavior and metabolism). Analysis of the way pigmentation and various other traits vary in mouse models leads to results consistent with this hypothesis.
A corollary of this argument is that in vertebrates where pigmentation is controlled downstream of the melanocortins (ie. at, or further downstream of, MC1R), this correlation between pigmentation and other traits should not be consistently true. For this reason, the authors argue that humans should be exempt. However, they may be unaware that some difference in pigmentation both between and within populations is controlled by ASIP, a protein that binds MC1R, acting as an antagonsist for melanocortin binding. Humans, then, could be an ideal test case for the hypothesis--do phenotypes like aggression map to ASIP like pigmentation does? However, the unpalatable nature of this question makes it rather unlikely to be pursued in humans.