Human Molecular Genetics Advance Access originally published online on November 3, 2008
Human Molecular Genetics 2009 18(3):405-417; doi:10.1093/hmg/ddn362
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Sex-specific roles of β-catenin in mouse gonadal development
1 Department of Veterinary Biosciences, University of Illinois at Urbana-Champaign, 3806 VMBSB, 2001 South Lincoln Avenue, Urbana, IL 61802, USA 2 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA
* To whom correspondence should be addressed. Tel: +1 2173339362; Fax: +1 2172441462; Email address: hhyao{at}illinois.edu
Received July 21, 2008; Accepted October 29, 2008
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) and Wnt4 knockout ovaries. In the absence of β-catenin, expression of Wnt4 was down-regulated while that of Rspo1 was not affected, placing β-catenin as a component in between Rspo1 and Wnt4. Our results demonstrate that β-catenin is responsible for transducing sex-specific signals in the SF1-positive somatic cell population during mouse gonadal development.
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