Follistatin operates downstream of Wnt4 in mammalian ovary organogenesis

Authors

  • Humphrey H.C. Yao,

    1. Department of Cell Biology, Duke University Medical Center, Durham, North Carolina
    Current affiliation:
    1. Department of Veterinary Biosciences, University of Illinois at Urbana-Champaign, IL
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  • Martin M. Matzuk,

    1. Departments of Pathology, Molecular and Cellular Biology, Molecular and Human Genetics, and Program in Developmental Biology, Baylor College of Medicine, Houston, Texas
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  • Carolina J. Jorgez,

    1. Departments of Pathology, Molecular and Cellular Biology, Molecular and Human Genetics, and Program in Developmental Biology, Baylor College of Medicine, Houston, Texas
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  • Douglas B. Menke,

    1. Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts
    Current affiliation:
    1. Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA
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  • David C. Page,

    1. Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts
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  • Amanda Swain,

    1. Institute of Cancer Research, Chester Beatty Laboratories, London, United Kingdom
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  • Blanche Capel

    Corresponding author
    1. Department of Cell Biology, Duke University Medical Center, Durham, North Carolina
    • Department of Cell Biology, Duke University Medical Center, Durham, NC 27708
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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 TGFβ 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. Developmental Dynamics 230:210–215, 2004. © 2004 Wiley-Liss, Inc.

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