It’s hard out here for a vole

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I’m sure many here are familiar with the prairie vole – montane vole story regarding mammalian monogamy. Prairie voles are more monogamous than montane voles. The two types have different distributions of Arginine Vasopressin Receptor 1a (avpr1a) expression in the brain. In a Science paper a little over a year ago, Hammock and Young reported that the DNA upstream of the avpr1a gene in prairie voles contains a bunch of short tandem repeats (STRs), and that the number of these repeats tracked with receptor distribution and with monogamous behavior. They also took a look at the DNA upstream of human, chimp, and bonobos and found repeat elements in common between humans and bonobos (more monogamous) that aren’t found in chimps (less monogamous). The implication is that tandem repeats work the same way in primates as in voles, and that polymorphisms here are directly linked to the complex behavior of monogamy.

It was a damn fine story, and it’s a shame to see it go, but check this PNAS paper out:

Mammalian monogamy is not controlled by a single gene.
Sabine Fink, Laurent Excoffier, and Gerald Heckel

Complex social behavior in Microtus voles and other mammals has been postulated to be under the direct genetic control of a single locus: the arginine vasopressin 1a receptor (avpr1a) gene. Using a phylogenetic approach, we show that a repetitive element in the promoter region of avpr1a, which reportedly causes social monogamy, is actually widespread in nonmonogamous Microtus and other rodents. There was no evidence for intraspecific polymorphism in regard to the presence or absence of the repetitive element. Among 25 rodent species studied, the element was absent in only two closely related nonmonogamous species, indicating that this absence is certainly the result of an evolutionarily recent loss. Our analyses further demonstrate that the repetitive structures upstream of the avpr1a gene in humans and primates, which have been associated with social bonding, are evolutionarily distinct from those in rodents. Our evolutionary approach reveals that monogamy in rodents is not controlled by a single polymorphism in the promoter region of the avpr1a gene. We thus resolve the contradiction between the claims for an evolutionarily conserved genetic programming of social behavior in mammals and the vast evidence for highly complex and flexible mating systems.

The paper makes two major points:

  1. There are a whole lot of non-monogamous vole species missing the STRs.
  2. The STRs in primates are about 5X further away from the avpr1a gene, and they are repeats of a different motif.

While there is still room for the STRs to modulate behavior one way or another, this report seems really damaging to the notion that arginine vasopressin receptor expression is a central component.


  1. I recently talked to a guy in a lab at UCSD who said they had tried to look in other species (I thought it was just the lab rat) and came to the conclusion that the tandem repeats were just in vole and the chimps.  
    I guess the STRs are in plenty of species, but to no effect. I wouldn’t say this necessarily degates the Larry Young work, it just means mating behavior is more complicated across the Class Mammalia than maybe Young was hoping for (whoop-see!). 
    All in all: two points each for positive and negative controls.

  2. ??the number of repeats tracked with receptor distribution?? 
    The repeats may be determining where the receptors are located? That is interesting. Has anyone worked out how that may be happening? 
    If I remember correctly, short terminating repeats are prone to copying errors so they should be hot spots for mutation. If the repeats are controlling the location and level of protein expression that would fit with a model of adaptation occurring primarily through changes in regulation of protein expression. 
    Are there other examples of repeats being linked to protein expression? 
    I wonder if this is related to packing DNA around histones: 
    Scientists discover a genetic code for organizing DNA within the nucleus 

  3. I’m not surprised that a behavioral trait as complex as monogamous mating requires several genes. It may be that monogamy is difficult to “achieve” in that many genes are necessary, but none is sufficient. Possibly in evolutionary lineages in which monogamy was selected for in the past, but not in the present, monogamous behavior was “re-lost” through a single gene mutation, making it seem as if only that gene is involved when performing comparisons, as the authors point out.