Last week I started to mention a recent paper in Nature on the evolution of malaria resistance in baboons, but then went out and partied instead. Not wanting to be a bastard, I’d better make good. While I’ll try to pull a good lesson from this, be warned that I’m about to discuss a topic about which I am no expert.

Malaria sucks, you don’t want to get it. There are anti-malaria medications out there, but I understand that they can make you insane, or at least have crazy dreams. Fortunately for millions of humans, there is a genetic basis for malaria resistance, so they don’t have to buy the anti-malaria crazy pills. Now, the paper tells me that a polymorphism in part of the FY gene turns the gene off in red blood cells, and that individuals with this variant are then strongly protected from malaria. No Lariam for these folks.

Jenny Tung and colleagues analyzed the homologous region of the FY gene in almost 200 yellow baboons (Papio cynocephalus) from Kenya, as well as tested these baboons for Hepatocystis parasites–relatives of Plasmodium vivax, which don’t cause malaria in baboons, but does really suck for them. And wouldn’t you know it–this same region on the baboon FY gene is also associated with Hepatocystis infection, where individuals with certain genetic variants have a lower susceptability to infection!

Now, the underlying genetic architecture and subsequent mechanisms of infection resistance are not exactly the same. But here’s the take home message from the paper:

“These results suggest that the genetic basis of phenotypic variation in different primate species can exhibit a remarkable degree of parallelism. In this case, not only are the similarities present at the molecular level . . . but they also extend to the mechanism that links molecular and phenotypic variation”

In other words, closely related species are equiped with very similar (or often the same) genetic or developmental “hardware,” and so evolution can cause them to come up with similar solutions to the same problem. In this case, there’s a similar genetic basis underlying infection resistance in humans and baboons. But I think this is a lesson that can be extended to, or at least kept in mind when considering, phenotypic evolution generally.

I’ve always (well, for the past three and a half years since I’ve been studying physical anthropology) thought that such a situation might characterize the “robust” australopithecines of East and South Africa. It is possible that these groups are not each others’ closest relatives, but that they evolved many craniodental characters in parallel, in response to selection for a heavy-chewing diet. This becomes even more plausible if it should turn out that many of these cranial and dental features are morphologically integrated–something I’m working on at the moment (if anyone reads this and scoops me, you will pay).

So, interesting paper. Reference

Tung, J. et al. Evolution of a malaria resistance gene in wild primates. Nature, in press.