Plasticity of the reproductive axis caused by social status change in an african cichlid fish: II. Testicular gene expression and spermatogenesis
Reproduction in all vertebrates is controlled by the brain-pituitary-gonad (BPG) axis, which is regulated socially in males of the African cichlid fish Astatotilapia burtoni.Althoughsocial information influences GnRH1 neurons at the apex of the BPG axis, little is known about how the social environment and dominance affects the cellular and molecular composition of the testes to regulate reproductive capacity. We created an opportunity for reproductively suppressed males to ascend in status and then measured changes in gene expression and tissue morphology to discover how quickly the perception of this opportunitycaninfluencethetestes.Ourresultsshowrapid up-regulation ofmRNAlevels ofFSH receptorandseveral steroid receptor subtypes inthetestesduringsocial ascent. In contrast,LHreceptor was not elevated until 72 h after ascent, but this increase was coincident with elevated circulating androgens and early stages of spermatogenesis, suggesting a role in steroidogenesis. The spermatogenic potential of the testes, as measured by cellular composition, was also elevated before the overall increase in testes size. The presence of cysts at all stages of spermatogenesis, coupled with lower levels of gonadotropin and steroid receptors in subordinate males, suggests that the BPG axis and spermatogenesis are maintained at a subthreshold level in anticipation of the chance to gain a territory and become reproductively active. Our results show that the testis is stimulated extremely quickly after perception of social opportunity, presumably to allow suppressed males to rapidly achieve high reproductive success in a dynamic social environment. Copyright © 2010 The Endocrine Society. All rights reserved.
Publication Source (Journal or Book title)
Maruska, K., & Fernald, R. (2011). Plasticity of the reproductive axis caused by social status change in an african cichlid fish: II. Testicular gene expression and spermatogenesis. Endocrinology, 152 (1), 291-302. https://doi.org/10.1210/en.2010-0876