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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.
1 Division of Genetics and Developmental Biology, Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia. 2 Australian Research Council Centre of Excellence in Biotechnology and Development, Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia. 3 Department of Oral Health Science, Faculty of Dentistry, University of British Columbia, Vancouver, BC V6T 1Z3, Canada. 4 Division of Molecular Biology, Institute for Molecular and Cellular Biology, Osaka University, and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Osaka 565-0871, Japan. 5 Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada.
* Present address: Faculty of Medicine, University of Ottawa,Ottawa, Ontario K1H 8M5, Canada.
Present address: Biochemistry Department, University of Otago,Post Office Box 56, Dunedin, New Zealand.
To whom correspondence should be addressed. E-mail: p.koopman{at}imb.uq.edu.au
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