The persistence of morphs

Science Daily has a summary of new fly research in behavioral genetics which puts the spotlight on deep time evolutionary dynamics. Here's the important bit:

The researchers found that when the fruit fly larvae were competing for food, those that did best had a version of the foraging gene that was rarest in a particular population. For example, rovers did better when there were lots of sitters, and sitters did better when there were more rovers.

In short the researchers here are pointing to negative frequency dependent selection, where traits/alleles exhibit a fitness as an inverse function of their frequency. This shouldn't be a surprise, the MHC loci are extremely polymorphic likely due in large part to frequency dependent effects. These genes are critical within the adaptive immune system of many "higher" organisms, an major line of defense against pathogens. Since pathogens evolve so quickly they can usually outfox common genetic profiles on these loci in short order, so what you generally see is a lot of diversity within a population on these loci precisely because rare allelic combinations are more likely to be a surprise for the various pathogen lines. The genetic homogeneity of Native American populations is one of the primary reasons they were so vulnerable to Eurasian pathogens, one strain which could outflank a population's modal immune strategy could wipe it out, just like crop monocultures can be swept away by infection.

But you knew this, or at least I hope you knew this. The utility of rare alleles so clear in regards to MHC that many of the lineages transcend the species barrier (because they never went extinct, remember that as they get more rare they can get increasingly more fit, buffering them from stochastic extinction events). Some of MHC lines are older than both chimpanzees and humans. This fact is relevant in regards to behavioral strategies. On my other blog I posted on work which suggests that one particular behavioral morph coded by the DRD4 gene might be as ancient at the vertebrate lineage! Two variant strategies might be extant within humans and birds. The same might be true of the gene in this study:

...The researchers' next step is to show that this phenomenon is also taking place in the wild. In addition, since the foraging gene is found in many animals, including honeybees, mice and humans, the researchers are examining how variations in the human foraging gene may be linked to food-related disorders.

Evolution is creative, but sometimes you just have to reinvent, or not lose, the wheel....

Note: The article will appear in today's Nature.

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Some of MHC lines are older than both chimpanzees and humans. This fact is relevant in regards to behavioral strategies. On my other blog I posted on work which suggests that one particular behavioral morph coded by the DRD4 gene might be as ancient at the vertebrate lineage!

Vertebrate, or amniote? :)

I don't see any indication in the article that *particular* morphs should be ancient, at least not in the same way that human MHC lineages are ancient.

They write: "These findings suggest that an association between Drd4 gene polymorphisms and animal personality variation predates the divergence of the avian and mammalian lineages."

I read this as: this gene is associated with a particular personality aspect in birds and mammals and thus their MRCA might be expected to have something similar. But there's no evidence that the novelty-seeking behaviour in birds and humans is homologous (sensu lato), and definitely not particular Drd4 alleles. Correct me if I'm wrong.

But there's no evidence that the novelty-seeking behaviour in birds and humans is homologous (sensu lato), and definitely not particular Drd4 alleles. Correct me if I'm wrong.

no, i think you're reading is right. i'm looking at phenotypic outcomes here though. there are many ways to lose function after all....

there are many ways to lose function after all....

Is novelty-seeking the function or the loss of function? :)

Is novelty-seeking the function or the loss of function? :)

you talking molecular mechanistically or behaviorally? ;-) the point is that i'm focusing to some extent on identity-by-phenotypic-outcome, not identity-by-descent or identity-by-state.