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Sexually dimorphic development of the gonads is controlled by positive and negative regulators produced by somatic cells. Many Wnt ligands, including ones that signal via the canonical β-catenin pathway, are expressed in fetal gonads. β-catenin, a key transcriptional regulator of the canonical Wnt pathway and an element of the cell adhesion complex, is essential for various aspects of embryogenesis. To study the involvement of β-catenin in sex determination, we ablated β-catenin specifically in the SF1-positive population of somatic cells. Although β-catenin was present in gonads of both sexes, it was necessary only for ovarian differentiation but dispensable for testis development. Loss of β-catenin in fetal testes did not affect Sertoli cell differentiation, testis morphogenesis or masculinization of the embryos. However, we observed molecular and morphological defects in ovaries lacking β-catenin, including formation of testis-specific coelomic vessel, appearance of androgen-producing adrenal-like cells and loss of female germ cells. These phenotypes were strikingly similar to those found in the R-spondin1 (Rspo1) andWnt4knockout ovaries. In the absence of β-catenin, expression ofWnt4was down-regulated while that ofRspo1was not affected, placing β-catenin as a component in betweenRspo1andWnt4. Our results demonstrate that β-catenin is responsible for transducing sex-specific signals in the SF1-positive somatic cell population during mouse gonadal development.

Sex-specific roles of β-catenin in mouse gonadal development