Retinoid signaling determines germ cell fate in mice

被引：729

作者：

Bowles, J

Knight, D

Smith, C

Wilhelm, D

Richman, J

Mamiya, S

Yashiro, K

Chawengsaksophak, K

Wilson, MJ

Rossant, J

Hamada, H

Koopman, P ^{[1
]}

机构：

[1] Univ Queensland, Div Genet & Dev Biol, Brisbane, Qld 4072, Australia

[2] Univ Queensland, Australian Res Council Ctr Excellence Biotechnol, Inst Mol Biosci, Brisbane, Qld 4072, Australia

[3] Univ British Columbia, Fac Dent, Dept Oral Hlth Sci, Vancouver, BC V6T 1Z3, Canada

[4] Osaka Univ, Inst Mol & Cellular Biol, Div Mol Biol, Suita, Osaka 5650871, Japan

[5] Japan Sci & Technol Corp, CREST, Suita, Osaka 5650871, Japan

[6] Hosp Sick Children, Toronto, ON M5G 1X8, Canada

来源：

SCIENCE | 2006年 / 312卷 / 5773期

关键词：

D O I：

10.1126/science.1125691

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：596 / 600

页数：5

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