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β-Catenin is essential for Müllerian duct regression during male sexual differentiation
Author(s) -
Akio Kobayashi,
C. Allison Stewart,
Ying Wang,
Kaoru Fujioka,
Nicholas Thomas,
Soazik P. Jamin,
Richard R. Behringer
Publication year - 2011
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.056143
Subject(s) - anti müllerian hormone , mullerian ducts , wnt4 , biology , wnt signaling pathway , medicine , endocrinology , mesenchyme , sexual differentiation , beta catenin , duct (anatomy) , müllerian mimicry , sox9 , signal transduction , microbiology and biotechnology , hormone , transcription factor , genetics , anatomy , embryo , gene , ecology
During male sexual differentiation, the transforming growth factor-β (TGF-β) signaling molecule anti-Müllerian hormone (AMH; also known as Müllerian inhibiting substance, MIS) is secreted by the fetal testes and induces regression of the Müllerian ducts, the primordia of the female reproductive tract organs. Currently, the molecular identity of downstream events regulated by the AMH signaling pathway remains unclear. We found that male-specific Wnt4 expression in mouse Müllerian duct mesenchyme depends upon AMH signaling, implicating the WNT pathway as a downstream mediator of Müllerian duct regression. Inactivation of β-catenin, a mediator of the canonical WNT pathway, did not affect AMH signaling activation in the Müllerian duct mesenchyme, but did block Müllerian duct regression. These data suggest that β-catenin mediates AMH signaling for Müllerian duct regression during male sexual differentiation.

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