Submitted October 9, 2007
Returned for revision November 7, 2007
Accepted January 4, 2008
Mechanisms of Hormone Action
Rainbow Trout Gonadal Masculinization Induced by Inhibition of Estrogen Synthesis Is More Physiological Than Masculinization Induced by Androgen Supplementation
Denise Vizziano ,
Daniel Baron ,
Gwenaëlle Randuineau ,
Sophie Mahé ,
Chantal Cauty ,
and
Yann Guiguen *
* To whom correspondence should be addressed. E-mail: yann.guiguen{at}rennes.inra.fr.
Abstract
The present study was designed to obtain new insights into fish gonadal sex differentiation by comparing the effects of two different masculinizing treatments on some candidate gene expression profiles. Masculinization was induced in rainbow trout, Oncorhynchus mykiss genetic all-female populations using either an active fish androgen (11betaAnd, 11beta-hydroxyandrostenedione) or an aromatase inhibitor (ATD, 1,4,6-androstatriene-3,17-dione). The expression profiles of 100 candidate genes were obtained by real-time RT-PCR and 46 profiles displayed a significant differential expression between control populations (males and females) and ATD / 11betaAnd-treated populations. These expression profiles were grouped in four temporally correlated expression clusters. Among the common responses shared by the two masculinizing treatments, the inhibition of some early female differentiating genes (cyp19a1, foxl2a, fst, fshb) appears to be crucial for effective masculinization, suggesting that these genes act together via a short regulation loop to maintain high sex-specific ovarian expression of cyp19a1. This simultaneous down-regulation of female specific genes could be triggered by some testicular genes such as dmrt1, nr0b1 (also known as dax1) and pdgfra, which are quickly up-regulated by the two masculinizing treatments. In contrast to 11betaAnd, ATD quickly restored the expression levels of steroidogenesis related genes (cyp11b2.1, cyp11b2.2, hsd3b1, cyp17a, star, nr5a1) and some Sertoli cell markers (sox9a2, amh) to the expression levels observed during control testicular differentiation. This demonstrates that these genes are probably not needed for active masculinization, and that the inhibition of endogenous estrogen synthesis produces a much more complete and specific testicular pattern of gene expression than that observed following androgen-induced masculinization.
Key words:
Ovary •
Testis •
Early development •
Gene regulation •
Steroid hormones
