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In mammals, male sex determination is governed by SRY-dependent activation of  Sox9 , whereas female development involves R-spondin1 (RSPO1), an activator of the WNT/beta-catenin signaling pathway. Genetic analyses in mice have demonstrated  Sry  and  Sox9  to be both required and sufficient to induce testicular development. These genes are therefore considered as master regulators of the male pathway. Indeed, female-to-male sex reversal in XX  Rspo1  mutant mice correlates with  Sox9  expression, suggesting that this transcription factor induces testicular differentiation in pathological conditions. Unexpectedly, here we show that testicular differentiation can occur in XX mutants lacking both  Rspo1  and  Sox9  (referred to as XX  Rspo1 KO Sox9 cKO    ) , indicating that  Sry  and  Sox9  are dispensable to induce female-to-male sex reversal. Molecular analyses show expression of both  Sox8  and  Sox10 , suggesting that activation of  Sox  genes other than  Sox9  can induce male differentiation in  Rspo1 KO Sox9 cKO   mice. Moreover, since testis development occurs in XY  Rspo1 KO Sox9 cKO   mice, our data show that  Rspo1  is the main effector for male-to-female sex reversal in XY  Sox9 cKO   mice. Thus,  Rspo1  is an essential activator of ovarian development not only in normal situations, but also in sex reversal situations. Taken together these data demonstrate that both male and female sex differentiation is induced by distinct, active, genetic pathways. The dogma that considers female differentiation as a default pathway therefore needs to be definitively revised.

Testicular Differentiation Occurs in Absence of R-spondin1 and Sox9 in Mouse Sex Reversals