Meeting Abstract
The production of many secondary sexual signals, including pheromones, is controlled by sex hormone action at the sites of signal synthesis. The red-garter snake (Thamnophis sirtalis parietalis) is an ideal vertebrate for studying the interaction between steroids and sexual signals: males exclusively rely on skin-based female pheromones during courtship and pheromone composition is augmented by treatment with sex steroids (e.g., males produce female pheromone if implanted with estrogen). But how do steroid hormones promote pheromone expression at the molecular level in snake skin? Feminizing effects of estrogens on sexual signals are known to result from activation of estrogen receptors α (ESR1) and/or β (ESR2), while masculinizing effects of androgens arise from androgen receptor (AR) activation. We hypothesized that ESR1, ESR2, and AR are expressed in garter snake skin but their expression is sex-dependent with female skin expressing higher levels of ESRs and males higher expression of AR. To test this, red-sided garter snakes (n=10 males, n=10 females) were collected in the spring mating season, and mRNAs from skin and control tissues (liver, gonad, kidney, intestine) were extracted and used to synthesize cDNAs. Primers were designed using the available T. sirtalis genome (NCBI) and tested in real-time PCR reactions. While all three receptor types were expressed in male and female skin, ESR1 was more highly expressed in female skin while AR showed greater expression in male skin. We thus attribute the feminizing effect of estrogen on pheromone phenotype in males to their lack of circulating estrogen and subsequently dormant ESRs. Further, activated AR may have an antagonistic role in pheromone expression since testosterone is a known inhibitor of pheromone production in male garter snakes.
