Ovarian control of growth and sexual size dimorphism in a male-larger gecko.

Sexual size dimorphism (SSD) reflects sex-specific solutions to the allocation of energy among growth, reproduction and survival; however, the proximate mechanisms behind these solutions are still poorly known even in vertebrates. In squamates, sexual differences in body size used to be attributed to direct energy allocation to energetically demanding processes, largely to reproduction. In addition, SSD is assumed to be controlled by specific endogenous mechanisms regulating growth in a sex-specific manner, namely masculinization by male gonadal androgens or feminization by ovarian hormones. We performed a manipulative growth experiment in females of the male-larger gecko in order to test the reproductive cost hypothesis, the male androgen hypothesis and the ovarian hormone hypothesis. Specifically, we investigated the effect of total ovariectomy, prepubertal ovariectomy, unilateral ovariectomy, and total ovariectomy followed by exogenous estradiol, dihydrotestosterone or testosterone treatment, on female growth in comparison to males and reproductively active females. The present results and the results of our previous experiments do not support the hypotheses that SSD reflects direct energy allocation to reproduction and that male gonadal androgens are involved. However, all lines of evidence, particularly the comparable growth of reproducing intact and unilaterally ovariectomized females, were concordant with the control of SSD by ovarian hormones. We suggest that feminization of growth by female gonadal hormones should be taken into consideration as an endogenous pathway responsible for the ontogeny of SSD in squamates.