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Submitted on February 1, 2006
Accepted on March 23, 2006
Retinoid Signaling Determines Germ Cell Fate in Mice
Josephine Bowles 1, Deon Knight 1, Christopher Smith 2, Dagmar Wilhelm 1, Joy Richman 3, Satoru Mamiya 4, Kenta Yashiro 4, Kallayanee Chawengsaksophak 5, Megan J. Wilson 6, Janet Rossant 5, Hiroshi Hamada 4, Peter Koopman 7*
1 Division of Genetics and Developmental Biology 2 Division of Genetics and Developmental Biology; Present address: Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada, K1H 8M5 3 Division of Genetics and Developmental Biology; Department of Oral Health Science, Faculty of Dentistry, University of British Columbia, Vancouver, BC, Canada V6T 1Z3 4 Division of Molecular Biology, Institute for Molecular and Cellular Biology, Osaka University, and CREST Japan Science and Technology Corporation (JST), Osaka, Japan 565-0871 5 The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8 6 Division of Genetics and Developmental Biology; Present address: Biochemistry Department, University of Otago, PO Box 56, Dunedin, New Zealand. 7 Division of Genetics and Developmental Biology; ARC Centre of Excellence in Biotechnology and Development, Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia.
* To whom correspondence should be addressed.
Peter Koopman , E-mail: p.koopman{at}imb.uq.edu.au
Germ cells in the mouse embryo can develop as oocytes or spermatogonia,depending on molecular cues that have not been identified. Wefound that retinoic acid, produced by mesonephroi of both sexes,causes germ cells in the ovary to enter meiosis and inititateoogenesis. Meiosis is retarded in the fetal testis by the actionof the retinoid-degrading enzyme CYP26B1, ultimately leadingto spermatogenesis. In testes of Cyp26b1-knockout mouse embryos,germ cells enter meiosis precociously, as if in a normal ovary.Thus, precise regulation of retinoid levels during fetal gonaddevelopment provides the molecular control mechanism that specifiesgerm cell fate.
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