Retinoid signaling determines germ cell fate in mice
Retinoid signaling determines germ cell fate in mice
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DOI：
10.1126/science.1125691
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发表时间：
2006-04-28
期刊：
影响因子：
56.9
通讯作者：
Koopman, P
中科院分区：
文献类型：
--
作者：
Bowles, J;Knight, D;Koopman, P
小鼠胚胎中的生殖细胞可发育为卵母细胞或精原细胞，这取决于尚未明确的分子信号。我们发现，由两性的中肾产生的视黄酸会使卵巢中的生殖细胞进入减数分裂并启动卵子发生。在胎儿睾丸中，由于视黄酸降解酶CYP26B1的作用，减数分裂受阻，最终导致精子发生。在Cyp26b1基因敲除的小鼠胚胎的睾丸中，生殖细胞过早地进入减数分裂，就像在正常卵巢中一样。因此，在胎儿性腺发育过程中对视黄酸水平的精确调控提供了决定生殖细胞命运的分子控制机制。
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.