Abstract
The Y chromosome gene Sry is responsible for sex determination in mammals. It acts briefly during fetal development and induces the development of testes rather than ovaries by turning on the expression of its autosomal downstream target Sox9. The activation of Sox9 in the absence Sry is sufficient for the initiation of male specific sex determination but the effects of such replacement on adult male fertility remain unclear. Here we tested for Sry-to-Sox9 replacement effects on spermatogenesis and fertility by examining transgenic mice with deleted endogenous Sry and testis determination driven by either Sry or Sox9 transgene, and comparing them to males with an intact Y chromosome.
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