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Background  Partial loss of function of the transcription factor  FOXL2  leads to premature ovarian failure in women. In animal models,  Foxl2  is required for maintenance, and possibly induction, of female sex determination independently of other critical genes, e.g.,  Rspo1 . Here we report expression profiling of mouse ovaries that lack  Foxl2  alone or in combination with  Wnt4  or  Kit / c-Kit .    Results  Following  Foxl2  loss, early testis genes (including  Inhbb, Dhh , and  Sox9 ) and several novel ovarian genes were consistently dysregulated during embryonic development. In the absence of  Foxl2 , expression changes affecting a large fraction of pathways were opposite those observed in  Wnt4 -null ovaries, reinforcing the notion that these genes have complementary actions in ovary development. Loss of one copy of  Foxl2  revealed strong gene dosage sensitivity, with molecular anomalies that were milder but resembled ovaries lacking both  Foxl2  alleles. Furthermore, a  Foxl2  transgene disrupted embryonic testis differentiation and increased the levels of key female markers.    Conclusion  The results, including a comprehensive principal component analysis, 1) support the proposal of dose-dependent  Foxl2  function and anti-testis action throughout ovary differentiation; and 2) identify candidate genes for roles in sex determination independent of  FOXL2  (e.g., the transcription factors IRX3 and ZBTB7C) and in the generation of the ovarian reserve downstream of  FOXL2  (e.g., the cadherin-domain protein CLSTN2 and the sphingomyelin synthase SGMS2). The gene inventory is a first step toward the identification of the full range of pathways with partly autonomous roles in ovary development, and thus provides a framework to analyze the genetic bases of female fertility.

Foxl2functions in sex determination and histogenesis throughout mouse ovary development