In the embryonic gonads of mice, the genetic and epigenetic regulatory programs for germ cell sex specification and meiosis induction or suppression are intertwined. The quest for garnering comprehensive understanding of these programs has led to the emergence of retinoic acid (RA) as an important extrinsic factor, which regulates initiation of meiosis in female fetal germ cells that have attained a permissive epigenetic ground state. In contrast, germ cells in fetal testis are protected from the exposure to RA due to the activity of CYP26B1, an RA metabolizing enzyme, which is highly expressed in fetal testis. In this review, we provide an overview of the molecular mechanisms operating in fetal gonads of mice, which enable regulation of meiosis via RA signaling.

中文翻译：

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维甲酸信号在小鼠胚胎发育过程中对减数分裂的调控。

在小鼠的胚胎性腺中，生殖细胞性别规范和减数分裂诱导或抑制的遗传和表观遗传调控程序相互交织。为了寻求对这些程序的全面理解，导致了视黄酸（RA）的出现，它是一种重要的外在因子，它调节已达到允许表观遗传基础状态的女性胎儿生殖细胞减数分裂的启动。相反，由于CYP26B1（一种在胎儿睾丸中高度表达的RA代谢酶）的活性，可以保护胎儿睾丸中的生殖细胞免于暴露于RA。在这篇综述中，我们提供了在小鼠胎儿性腺中起作用的分子机制的概述，这些分子机制能够通过RA信号调节减数分裂。