Genetic polymorphisms in wild baboons

ResearchBlogging.orgUpdate:  As it turns out, John Hawks wrote a post about this, too, and since he’s much better versed in genetics than I am, I’ll point you over to his place for a additional, and better, coverage of this paper.

Malaria is one of the most common infectious diseases around.  It’s caused by little Plasmodium protozoans that are transmitted by the Anopheles mosquito.  The female mosquito picks up the protozoans from one host, and then, once the parasites have made it up into her salivary glands, she is able to inject the parasites into another animal.  Once in the new host, most strains of malaria travel to the liver, where they differentiate and multiply until their host cells burst.  Then, they leave the liver to infect the red blood cells, where they differentiate, eat, and reproduce.  Malaria can be deadly in many cases, particularly with Plasmodium falciparum, and extremely unpleasant when not fatal.  Since it’s so deadly and common, malaria has been a rather strong selective pressure throughout human evolution.  Sickle-cell diseases, which “starve” the protozoans, have become extremely common in human populations which are at risk for P. falciparum. Heterozygotes for the trait are at a particular advantage, since many of their blood cells function normally.  Likewise with thalassemias, which muck up the beta chain of hemoglobin in the red blood cell and make it harder for the protozoan to find a nice, comfy cell in which to grow.

We know quite a bit about genetic traits and their effect on malaria transmission.  Just ask any undergrad who’s taken a class in human variation!  However, we know very little about these things in wild primates.  Jenny Tung and her colleagues sought to remedy that by studying a population of wild baboons (Papio cynocephalus) at Amboseli National Park in Kenya.

Tung studied the FY gene, which codes for a chemokine receptor on the surface of the red blood cells.  This receptor is often the point on the cell surface through which Plasmodium vivax enters.  In humans, there is one polymorphic locus in the cis-regulatory region of FY. Normally, a thymine (T) is coded for at this locus. In humans in which cytosine (C) is coded instead, the chemokine receptor is not expressed, and P. vivax can’t enter the cell.  Homozygotes for the C variant are especially protected, and heterozygotes exhibit mild protection. The C variant has achieved high frequencies in two different haplogroups in Africa, which suggests that it’s being selected for in regions where P. vivax is a problem.  Baboons aren’t usually infected by Plasmodium protozoans, but they are particularly susceptible to a slightly different protozoan, Hepatocystis kochi, which behaves almost exactly as the Plasmodium protozoan behaves in humans.

At Amboseli, 61.9% of the baboon population tested had H. kochi, but there was quite a bit of variation between different social groups.  Tung and her colleagues also sequenced a region of DNA in the baboons which was homologous to our FY cis-regulatory region.  They found six single nucleotide polymorphisms (SNPs).  At one particular polymorphism site, some of the baboons expressed adenine (A), while the others expressed guanine (G).  The risk of Hepatocystis infection within a population decreased as the number of G alleles in the population increased.

Of course, any student of statistics will tell you that correlation does not equal causation!  To test whether this polymorphism site was affecting the expression of any genes, such as those coding for the chemokine receptor in humans, they measured allele-specific expression of the genes using pyrosequencing.  They used DNA from heterozygote individuals to see if there was a difference in how the alleles were expressing FY. All of the polymorphisms showed variation in expression of the gene.  This suggests that the same mechanisms which have acted during human evolution to reduce malaria susceptibility may also be acting in other primates.  However, while mechanism is pretty much the same- change the way in which the chemokine receptor is expressed so that the parasite has a harder time invading the cell- the ways in which we have gone about doing that are different.  In humans, the polymorphism is Mendelian.  You either have the receptor, or you don’t.  In baboons, it’s a polygenic trait.  Lots of different sites in the cis-regulatory region of FY are acting to influence the expression of that receptor.

This is an important step forward in the study of wild primates.  We know lots about their ecology, behavior, and morphology, but our knowledge of their genetics comes from captive primates.  This paper shows that it’s important to look at the wild populations, too, because they might be able to tell us about variation within the species.  And, they’ll be able to tell us more about the selective pressures which may act on our own species.
Tung, J., Primus, A., Bouley, A., Severson, T., Alberts, S., & Wray, G. (2009). Evolution of a malaria resistance gene in wild primates Nature DOI: 10.1038/nature08149

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2 responses to “Genetic polymorphisms in wild baboons

  1. Moebius July 6, 2009 at 6:47 pm

    Terrific review. I just came across it at Scientia Pro Publica. I’m sure Susan would be pleased. I linked to this post here.

  2. zinjanthropus July 6, 2009 at 11:29 pm

    Thanks for the link! I had just added your blog to my blogroll the day before your move to scienceblogs! Thanks for reminding me to switch it around…

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