Retinoid Signaling Determines Germ Cell Fate in Mice

Author:

Bowles Josephine12345,Knight Deon12345,Smith Christopher12345,Wilhelm Dagmar12345,Richman Joy12345,Mamiya Satoru12345,Yashiro Kenta12345,Chawengsaksophak Kallayanee12345,Wilson Megan J.12345,Rossant Janet12345,Hamada Hiroshi12345,Koopman Peter12345

Affiliation:

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.

Abstract

Germ cells in the mouse embryo can develop as oocytes or spermatogonia, depending on molecular cues that have not been identified. We found that retinoic acid, produced by mesonephroi of both sexes, causes germ cells in the ovary to enter meiosis and inititate oogenesis. Meiosis is retarded in the fetal testis by the action of the retinoid-degrading enzyme CYP26B1, ultimately leading to 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 gonad development provides the molecular control mechanism that specifies germ cell fate.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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