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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: J Androl. 2009 Oct 29;31(1):16–25. doi: 10.2164/jandrol.109.008201

Figure 3.

Figure 3

Model of sex determination in mammals. Sry begins to be expressed in somatic cells around 10.5 dpc (days post coitum) and immediately induces the activation of Sox9, followed by the expression of a cascade of testis-specific markers that direct the development of the testis from the bipotential gonad in XY individuals. In the female, where Sry is not present, Foxl2, Rspo1 and other ovarian genes begin to be expressed around 11.5 dpc, i.e., at the same time at which Sry and Sox9 have reached their maximal levels in the male gonad. It represses the expression of Sox9, and along with other female markers leads to the development of the ovary. If Foxl2 is inactivated (red X), Sox9 is turned on, possibly by a putative “M” factor (see text), and somatic cells begin to differentiate along the testis pathway, resulting in a sex reversal that is only partial in mice. XX germ cells follow an independent pathway, characterized by the colonization of the gonad and entry into meiosis before somatic cell sex reversal is complete. Though sex choice of the germ cell lineage is resistant to the individual loss of Foxl2 in mice, this is at least partly due to the persistent action of other ovarian somatic genes, including Rspo1 and Wnt4, The nature and functional relevance of inductive interactions among distinct female cell lineages during early ovary differentiation is still poorly understood. Hammered blue lines indicate antagonistic interactions.