Meeting Abstract
Understanding how different phenotypes develop from the same underlying genome is an important goal of integrative biology. Males and females share an autosomal genome, which may constrain the development of sexual dimorphism. Developmental modifiers such as sex steroids, which are secreted in sex-specific fashion, can facilitate the development of sexual dimorphism by differentially regulating the expression of shared autosomal loci. However, it is generally unknown whether the evolution of endocrine-mediated sexual dimorphism is achieved primarily through sex differences in circulating hormones, or also through sex-specific tissue sensitivity to these hormones. We tested the effect of the sex steroid testosterone (T) on whole-organism growth and tissue-specific gene expression of the liver (a major integrator of energetics and growth) in males and females of a lizard (Anolis sagrei) with pronounced male-biased sexual size dimorphism. We administered either testosterone or placebo implants to intact males and females at the age (5-6 mo) when sexual dimorphism first becomes pronounced. T shifted both sexes toward a male-specific pattern of development by stimulating growth, bone elongation, resting metabolic rate, and utilization of fat reserves. The transcriptome of the liver was similarly impacted by T, which shifted both sexes towards a male-specific pattern of gene expression that included altered regulation of genes in the insulin-like growth factor (IGF-1) pathway. Our results suggest that the evolution of endrocrine-mediated sexual dimorphism in growth and body size is achieved primarily through sex differences in circulating androgen levels, rather than through a reduction in sensitivity of females to androgens.
