1Structural Biology, Stanford University School of Medicine, 2Vaccine Research Center, National Institutes of Health, 3Medicine and Microbiology, Perelman School of Medicine, University of Pennsylvania, 4Evolutionary Anthropology, Duke University
Saturday 11:30-11:45, 200ABC
The highly polymorphic genes of the Major Histocompatibility Complex (MHC) are of interest for their immunological role in antigen presentation to T-cells and natural killer (NK) cells, and also for their effect in mate-choice and reproductive success. Understanding how this gene complex evolves is essential to understanding its function and evolutionary trajectory. Consequently research has investigated these genes in non-human primates, particularly chimpanzees, but relied on samples from captive animals. Although we now have good understanding of how MHC genes work at the level of the individual, we do not understand their distribution at the population level because captive chimpanzees unlikely represent the natural variation in the wild. Thus, basic but crucial questions remain unanswered concerning the quantity and quality of the MHC diversity maintained by wild chimpanzee populations. Therefore, we conducted this study of the wild Eastern chimpanzee population (Pan troglodytes schweinfurthii) of Gombe National Park, Tanzania, a subspecies underrepresented in captive populations. Using DNA isolated from feces, we sequenced 119 individuals for the MHC-B gene (Patr-B) and detected 11 alleles. Seven of the alleles were novel and differed from other alleles by amino-acid altering mutations at immunologically important sites. Furthermore, one or two alleles are maintained at high frequency (≥30%), whereas the others are maintained at much lower frequencies (≤ 15%). This pattern of allele number and frequency is comparable to that found in tribal human populations, suggesting it represents the base level of MHC-B diversity necessary to maintain a healthy and naturally reproducing chimpanzee or human population.
The project was funded primarily by the National Institutes of Health (NIH) (grant no. R01 AI031168). Genetic analyses were supported by grants from the NIH (R01 AI50529, R01 AI58715, P30 AI 27767) and Wroblewski was supported by a Ruth L. Kirschstein National Research Service Award (NIH F32 AI085959-03).