Androgens regulate sex differences in signaling but are not associated with male variation in morphology in the weakly electric fish Parapteronotus hasemani

Abstract

Sexually dimorphic signaling is widespread among animals and can act as an honest indicator of mate quality. Additionally, differences in signaling and morphology within a sex can be associated with different strategies for acquiring mates. Weakly electric fish communicate via self-generated electrical fields that transmit information about sex, reproductive state, and social status. The weakly electric knifefish Parapteronotus hasemani exhibits sexual dimorphism in body size as well as substantial within-male variation in body size and jaw length. We asked whether P. hasemani exhibits hormonally mediated sexual dimorphism in electrocommunication behavior. We also asked whether males with short versus long jaws differed significantly from each other in morphology, behavior, hormone levels, or reproductive maturity. Males produced longer chirps than females, but other signal parameters (electric organ discharge frequency; chirp rate and frequency modulation) were sexually monomorphic. Pharmacologically blocking androgen receptors in males reduced chirp duration, suggesting that this sexually dimorphic trait is regulated at least in part by the activational effects of androgens. Males sorted into two distinct morphological categories but did not differ in circulating 11-ketotestosterone or testosterone. Short-jawed males and long-jawed males also did not differ in any aspects of signaling. Thus, chirping and high levels of 11-ketotestosterone were reliably associated with reproductively active males but do not necessarily indicate male type or quality. This contrasts with other alternative male morph systems in which males that differ in morphology also differ in androgen profiles and signaling behavior.

Genes linked to species diversity in a sexually dimorphic communication signal in electric fish

“…Variation in sexual dimorphism of EODf is linked to variation in the sensitivity of this signal to gonadal steroid hormones. Sex differences in EODf in species with sexually dimorphic EODs are caused by effects of androgens and/or estrogens on this signal, whereas EODf is less responsive to these hormones in species and populations with reduced or no sex differences in EODf (Meyer et al 1987; Schaefer and Zakon 1996; Dunlap et al 1998; Ho et al 2013; Petzold and Smith 2016). Moreover, reversals in the direction of sex differences in EODf are mediated by reversals of androgenic regulation of EODf.…”