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Journal Article

Monogamy evolves through multiple mechanisms: evidence from V1aR in deer mice


Turner,  Leslie M.
Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Turner, L. M., Young, A. R., Römpler, H., Schöneberg, T., Phelps, S. M., & Hoekstra, H. E. (2010). Monogamy evolves through multiple mechanisms: evidence from V1aR in deer mice. Molecular Biology and Evolution, 27(6), 1269-1278. doi:10.1093/molbev/msq013.

Cite as:
Genetic variation in Avpr1a, the locus encoding the arginine vasopressin receptor 1A (V1aR), has been implicated in pair-bonding behavior in voles (genus Microtus) and humans, raising the possibility that this gene may contribute commonly to mating-system variation in mammals. In voles, differential expression of V1aR in the brain is associated with male partner-preference behavior in a comparison of a monogamous (Microtus ochrogaster) and promiscuous (Microtus montanus) species. This expression difference is correlated, in turn, with a difference in length of a 5' regulatory microsatellite in Avpr1a. Here, we use a combination of comparative sequencing of coding and regulatory regions, analysis of neural expression patterns, and signaling assays to test for differences in V1aR expression and function among eight species of deer mice (genus Peromyscus). Despite well-documented variation in Peromyscus social behavior, we find no association between mating system and length variation in the microsatellite locus linked to V1aR expression in voles. Further, there are no consistent differences in V1aR expression pattern between monogamous and promiscuous species in regions of the brain known to influence mating behavior. We do find statistical evidence for positive selection on the V1aR coding sequence including several derived amino acid substitutions in a monogamous Peromyscus lineage, yet these substitutions have no measurable effect on V1aR signaling activity. Together, these results suggest that mating-system variation in rodents is mediated by multiple genetic mechanisms.