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This Article Full Text Full Text (PDF) [Supplemental Table] All Versions of this Article: 78/5/939    most recent biolreprod.107.065961v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Vizziano, D. Articles by Guiguen, Y. PubMed PubMed Citation Articles by Vizziano, D. Articles by Guiguen, Y. Agricola Articles by Vizziano, D. Articles by Guiguen, Y.

Rainbow Trout Gonadal Masculinization Induced by Inhibition of Estrogen Synthesis Is More Physiological Than Masculinization Induced by Androgen Supplementation¹

Facultad de Ciencias,³ Oceanología, Montevideo 11400, Uruguay INRA, SCRIBE,⁴ IFR 140, Cédex Rennes 65342, France

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, and 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, and nr5a1) and some Sertoli cell markers (sox9a2 and 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.

early development, gene regulation, ovary, steroid hormones, testis

¹Supported by the Institut National de la Recherche Agronomique (INRA) and a CIPA-OFIMER-INRA (AGENOP) grant. D.V. received financial support from CSIC (Universidad de la República of Uruguay) and a fellowship from the PHASE Animal Physiology and Breeding System INRA department.

Correspondence: ²FAX: 33 2 234 85020; e-mail: yann.guiguen{at}rennes.inra.fr