Yadu Nomesh, Kumar Pradeep G
Division of Molecular Reproduction, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, Kerala, India.
Genesis. 2019 Jul;57(7-8):e23327. doi: 10.1002/dvg.23327. Epub 2019 Jul 17.
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.
在小鼠胚胎性腺中，生殖细胞性别决定以及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。为全面理解这些程序，视黄酸（RA）作为一种重要的外在因子应运而生，它可调节已达到允许性表观遗传基态的雌性胎儿生殖细胞减数分裂的起始。相比之下，由于RA代谢酶CYP26B1在胎儿睾丸中高度表达，胎儿睾丸中的生殖细胞可免受RA的影响。在本综述中，我们概述了小鼠胎儿性腺中通过RA信号传导调控减数分裂的分子机制。
