Abstract # 6256 Poster # 205:

Scheduled for Friday, June 19, 2015 06:00 PM-08:00 PM: (Cascade AJBCD) Poster Presentation


N. D. Simons1, M. J. Ruiz-Lopez2, C. A. Chapman3,4, T. L. Goldberg4,5, K. N. Sterner1 and N. Ting1,2
1University of Oregon, Department of Anthropology, 308 Condon Hall, Eugene, OR 97403, USA, 2Institute of Ecology and Evolution, University of Oregon, 3Department of Anthropology and School of Environment, McGill University, 4Makerere University Biological Field Station, Makerere University, Uganda, 5Department of Pathobiological Sciences, University of Wisconsin-Madison
     Revealing immune processes that underlie genotype-phenotype associations will provide a better understanding of complex host-pathogen adaptation in non-human primates. While research in this area has primarily focused on protein-coding regions of the genome, the role of regulatory genetic variation in controlling an organism’s immune response to infectious disease remains largely unknown. To address this, we tested associations between the core promoters of two immune-related genes and gastro-intestinal helminth infection intensity in the Ugandan red colobus at Kibale National Park, Uganda. Our two candidate genes were IL-4 and MHC-DQA1, both of which have known associations with gastro-intestinal helminth infection, and we focused on the whipworm parasite (Trichuris), which has known fitness consequences in humans. We sequenced the core promoters of IL-4 and MHC-DQA1 in 31 Ugandan red colobus monkeys and reconstructed individual haplotypes. While the core promoter of IL-4 contained no variation, fifteen individual regulatory variants were identified in the functionally important transcription factor binding sites of the MHC-DQA1 core promoter. Genotypes for each SNP were tested for associations with whipworm infection intensity using a generalized linear model. Our results identified two functional regulatory variants associated with increased infection intensity for the heterozygote genotype (SNP-121, p = 0.007, and SNP-197, p = 0.012). This work highlights the importance of regulatory genetic variation in determining disease susceptibility and gene expression as an explanatory mechanism underlying disease association.