Dihydrotestosterone inhibits growth in a female-larger lizard (Sceloporus undulatus) implications for the development of sexual size dimorphism


Meeting Abstract

83-5  Wednesday, Jan. 6 11:00  Dihydrotestosterone inhibits growth in a female-larger lizard (Sceloporus undulatus): implications for the development of sexual size dimorphism POLLOCK, NB*; DRAZENOVIC, M; FEIGIN, SE; JOHN-ALDER, HB; Rutgers Univ., New Brunswick; Rutgers Univ., New Brunswick; Rutgers Univ., New Brunswick; Rutgers Univ., New Brunswick henry@aesop.rutgers.edu http://deenr.rutgers.edu/John-alder.html

Sexual size dimorphism (SSD) is widespread, and both male- and female-biased SSD occurs even within species lineages. Recent evidence indicates that testosterone (T) is a bipotential regulator of sex-specific growth rates contributing to the development of SSD in lizards, where T has opposite effects on growth in male- versus female-larger species. However, mechanisms behind these effects are not known. We previously reported that T inhibits growth in Sceoporus undulatus (Eastern Fence Lizard), in which females grow faster to become larger adults than males. Here, we test whether the growth-inhibitory effect of T can be replicated by dihydrotestosterone (DHT), which would suggest T acts via androgen receptors and not via aromatization of T to estradiol. We conducted laboratory experiments on yearling S. undulatus captured in their first full activity season at about ten months of age. We implanted Silastic tubules containing 150 microgram DHT into intact females and into intact and castrated males. Growth rates were measured for 40 days. We quantified dorsal and ventral colorations to corroborate treatment efficacies. Dihydrotestosterone inhibited growth in both females and males and caused the expression of male-typical coloration in females and castrated males. Feeding rate and body condition were unaffected by DHT, indicating that differences in growth rates were independent of energy balance. The present results suggest 1) that growth inhibition by T, which contributes to the development of SSD, is mediated by androgen receptors, and 2) that the T-regulatory network, including functional androgen receptors, is present in both sexes.

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