1. Prarie voles are socially monogomous (note the qualifier “socially”. Genetics suggests a certain amount of “infidelity”, if one can call it that in voles). Meadow voles are not.
2. There is a regulatory region upstream of the vasopressin receptor that carries a “short” allele in meadow voles and a “long” allele in prarie voles.
3. In vitro, the long and short alleles have higher and lower expression, respectively, of vasopressin.
4. When the prarie vole allele is transformed into meadow voles, there is as marked increase in pair bonding[cite]
5. Within prairie voles, different allele lengths are associated with pair bonding and vasopressin receptor distribution [cite]
This is a fascinating story, and many people, including the authors of the above papers, hypothesized a sort of single “switch” for monogamy in mammals. However,
6. Many non-monogamous species have “long” alleles [cite]
This, then, refutes the possibility of a single genetic switch controlling monogamy in mammals. The response just published in TIG accepts that, but argues against rejecting a role for vasopressin recepter variability in pair-bonding and other social behavior. I agree. The previous studies are quite convincing that such a role does exist (see in particular the experiments in the papers cited in points 4 and 5), and more detailed study of the vasopressin receptor locus is certainly justified.