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This Article Accepted manuscript (PDF) All Versions of this Article: JME-08-0039v1 41/5/277    most recent Alert me when this article is cited Alert me if a correction is posted Services 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-Cantonnet, D. Articles by Guiguen, Y. PubMed PubMed Citation Articles by Vizziano-Cantonnet, D. Articles by Guiguen, Y.

D Vizziano-Cantonnet, Facultad de Ciencias, Montevideo, Uruguay
D Baron, Universite de Nantes, Nantes, France
S Mahe, PHASE, INRA, Rennes, France
C Cauty, PHASE, INRA, Rennes, France
A Fostier, PHASE, INRA, Rennes, France
Y Guiguen, PHASE, INRA, Rennes, 35342, France

Correspondence: Yann Guiguen, Email: Yann.Guiguen{at}rennes.inra.fr

Abstract

In non-mammalian vertebrates, estrogens are key players in ovarian differentiation, but the mechanisms by which they act remain poorly understood. The present study on rainbow trout was designed to investigate whether estrogens trigger the female pathway by activating a group of early female genes (i.e. cyp19a1, foxl2a, foxl2b, fst, bmp4, and fshb) and by repressing early testicular markers (i.e. dmrt1, nr0b1 or dax1, sox9a1 and sox9a2). Feminization was induced in genetically all-male populations using 17alpha-ethynylestradiol (EE2, 20 mg/kg of food during two months). The expression profiles of 100 candidate genes were obtained by real-time RT-PCR and 45 expression profiles displayed a significant differential expression between control populations (males and females) and EE2-treated populations. These expression profiles were grouped in five temporally-correlated expression clusters. The estrogen treatment induced most of the early ovarian differentiation genes (foxl2a, foxl2b, fst, bmp4, and fshb) and in particular foxl2a, which was strongly and quickly up-regulated. Simultaneously, Leydig cell genes, involved in androgen synthesis, as well as some Sertoli cell markers (amh, sox9a2) were strongly repressed. However, in contrast with our initial hypothesis, some genes considered as essential for mammalian and fish testis differentiation were not suppressed during the early process of estrogen-induced feminization (dmrt1, nr0b1 or dax1, sox9a1 and pax2a) and some were even strongly up-regulated (nr0b1, sox9a1and pax2a). In conclusion, estrogens trigger male-to-female trans-differentiation by up-regulating most ovarian specific genes and this up-regulation appears to be crucial for an effective feminization, but estrogens do not concomitantly down-regulate all the testicular differentiation markers.