Meeting Abstract
The white-throated sparrow is powerful model in behavioral neuroendocrinology because it exhibits a chromosomal inversion (ZAL2m) that segregates with crown plumage and steroid-dependent behavior. Birds of the white-striped (WS) morph are heterozygous for the ZAL2m rearrangement and exhibit higher levels of vocal aggression than birds of the tan-striped (TS) morph, which are ZAL2 homozygotes. Recombination suppression between ZAL2 and ZAL2m has resulted in the divergence of captured genes, including ESR1, which encodes estrogen receptor alpha (ERα). ERα expression in the brain depends strongly on genotype and predicts territorial aggression. Here, we used complementary in vitro and in vivo approaches to test a model in which regulatory variation in ESR1 contributes to variation in aggression. First, we established that regulatory regions upstream of ESR1 contain fixed SNPs that occur in putative binding sites for transcription factors and CpG sites. Using a reporter assay, we found that the level of transcription depended on haplotype. Our results suggest that sequence divergence may explain the known morph differences in ERα expression in the brain. Next, we performed a behavioral study in which we manipulated estradiol (E2) levels. We reasoned that if the morph difference in ERα expression contributes to the behavioral polymorphism, then E2 should affect behavior more in one morph than the other. Exogenous E2 administration enhanced aggression in WS birds, but not TS birds, suggesting that the behavioral polymorphism may be mediated in part by differential sensitivity to E2. Taken together, our studies are consistent with the hypothesis that ESR1 contains SNPs that lead to morph differences in ERα expression and that in turn, those differences in expression mediate morph differences in vocal aggression.
