1Neuroscience, University of Pennsylvania, 2Evolutionary Anthropology, Duke University, 3Institute for Cognitive Science, University of Colorado, Boulder, 4Centre for Research in Animal Behaviour, University of Exeter, 5Duke Institute for Brain Sciences, Duke University, 6Biological and Biomedical Sciences, North Carolina Central University
April 21, 2017 , Studio 8/9/10
Evidence suggests that individual variation in social behavior arises from a combination of genetic predispositions and individual experience, yet the underlying biological mechanisms linking the two remain poorly understood. To address this gap, we seek to understand the genetic, developmental, and neurobiological contributions to social behavior in a population of rhesus macaques (Macaca mulatta) on Cayo Santiago island (Puerto Rico), which represents a large, free-ranging study sample with a known pedigree and well-characterized behavioral and cognitive phenotypes. We hypothesize that genetic variants underlying molecular differences in neuroreceptors are associated with distinct suites of behaviors in this socially complex species. To describe genetic variation, we generated whole genome sequences for 217 individuals using 100bp Illumina paired-end libraries. The population was sequenced to a total genome coverage of 1240X (mean 5.7X per individual), and the reads were then aligned to the rhesus macaque reference genome. We implemented variant detection and identified over nineteen million single nucleotide variants in the population. This total included 346,972 exonic variants, of which 40% were predicted to alter transcript splicing sites or the translated protein sequences. Regarding the latter, amino acid changes were described in dopamine receptors, oxytocin and vasopressin receptors, serotonin transporters, and the opioid receptor, mu-1 (OPRM1). We assessed the functional impact of these amino acid changes using computational tools that predict the potential damage of missense genetic mutations, finding neutral, tolerated and deleterious impacts on the receptor and transporter proteins. We posit that particular genetic variants within fundamental neurotransmitter pathways underlie social behavioral differences.
Funding support by NIH-NIMH R01 MH096875