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Steroid enzyme gene expression during natural and androgen-induced gonadal differentiation in the rainbow trout, Oncorhynchus mykiss

Govoroun M., McMeel O.M., D'Cotta H., Ricordel J.P., Smith T., Fostier A., Guiguen Y.. 2001. Journal of Experimental Zoology, 290 : p. 558-566.

DOI: 10.1002/jez.1106

In fish, according to Yamamoto's model, androgens would drive testis differentiation and estrogens ovarian differentiation. In order to study the implication of steroid enzymes in rainbow trout gonadal differentiation, we examined the expression of some steroid enzyme genes during natural differentiation (cholesterol side chain cleavage = P450scc, 17-hydroxylase/lyase = P450c17, 3ß-hydroxysteroid dehydrogenase = 3ßHSD) and androgen-induced differentiation (P450scc, P450c17 3ßHSD, aromatase = P450aro, and 11ß-hydroxylase = P45011ß). Expressions of P450scc, 3ßHSD, and P450c17 were all detected in male and female gonads at 55 days post-fertilization (dpf), i.e., two weeks before histological differentiation. There were no differences in their expression level respective to the sex. The androgen treatment was carried out by administration of 11ß-hydroxyandrostenedione (11ßOHA4) in genetic all-female populations and the resulting sex ratios were found to be 100% male even at a low dosage of 1 mg/kg of food. Following 11ßOHA4 treatment, only the expression of P450c17 was found to be sustained when compared with the female untreated control. In contrast, P450scc was clearly up-regulated and 3ßHSD and P450aro down-regulated by the androgen treatment. P45011ß gene expression remained low in gonads of androgen-ireated females, as it did in control untreated females. These results together demonstrate that steroidogenesis in rainbow trout is potentially active in predifferentiating gonads of both sexes, and that one of the masculinizing actions of androgens in the species may be to down-regulate the female-specific gonadal P450aro gene expression. However, in vivo androgen treatment in genetic females does not induce the same pattern of steroid gene expression as in genetic males. These data suggest that exogenous androgens might induce a male differentiation process with P450aro inhibition being one of the steps required. However, this process would not involve endogenously produced 11-oxygenated androgens.
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