<i>Follistatin</i> operates downstream of <i>Wnt4</i> in mammalian ovary organogenesis
Humphrey Hung‐Chang Yao(Duke Medical Center), Martin M. Matzuk(Baylor College of Medicine), Carolina J. Jorgez(Baylor College of Medicine), Douglas B. Menke(Howard Hughes Medical Institute), David C. Page(Howard Hughes Medical Institute), Amanda Swain(Institute of Cancer Research), Blanche Capel(Duke University)
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Abstract
Wnt4(-/-) XX gonads display features normally associated with testis differentiation, suggesting that WNT4 actively represses elements of the male pathway during ovarian development. Here, we show that follistatin (Fst), which encodes a TGFbeta superfamily binding protein, is a downstream component of Wnt4 signaling. Fst inhibits formation of the XY-specific coelomic vessel in XX gonads. In addition, germ cells in the ovarian cortex are almost completely lost in both Wnt4 and Fst null gonads before birth. Thus, we propose that WNT4 acts through FST to regulate vascular boundaries and maintain germ cell survival in the ovary.
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