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PRC1-mediated epigenetic programming is required to generate the ovarian reserve
Nature Communications ( IF 14.7 ) Pub Date : 2022-08-10 , DOI: 10.1038/s41467-022-31759-6
Mengwen Hu 1, 2 , Yu-Han Yeh 1, 2 , Yasuhisa Munakata 1, 2 , Hironori Abe 1, 2 , Akihiko Sakashita 2, 3 , So Maezawa 2, 4 , Miguel Vidal 5 , Haruhiko Koseki 6 , Neil Hunter 1, 7 , Richard M Schultz 8, 9 , Satoshi H Namekawa 1, 2
Affiliation  

The ovarian reserve defines the female reproductive lifespan, which in humans spans decades due to robust maintenance of meiotic arrest in oocytes residing in primordial follicles. Epigenetic reprogramming, including DNA demethylation, accompanies meiotic entry, but the chromatin changes that underpin the generation and preservation of ovarian reserves are poorly defined. We report that the Polycomb Repressive Complex 1 (PRC1) establishes repressive chromatin states in perinatal mouse oocytes that directly suppress the gene expression program of meiotic prophase-I and thereby enable the transition to dictyate arrest. PRC1 dysfuction causes depletion of the ovarian reserve and leads to premature ovarian failure. Our study demonstrates a fundamental role for PRC1-mediated gene silencing in female reproductive lifespan, and reveals a critical window of epigenetic programming required to establish ovarian reserve.



中文翻译:

产生卵巢储备需要 PRC1 介导的表观遗传编程

卵巢储备定义了女性的生殖寿命,由于原始卵泡中卵母细胞减数分裂停滞的稳健维持,人类的生殖寿命长达数十年。表观遗传重编程,包括 DNA 去甲基化,伴随减数分裂进入,但支持卵巢储备生成和保存的染色质变化尚不清楚。我们报告说,多梳抑制复合物 1 (PRC1) 在围产期小鼠卵母细胞中建立抑制染色质状态,直接抑制减数分裂前期-I 的基因表达程序,从而实现向 dictyate 停滞的过渡。PRC1 功能障碍导致卵巢储备耗尽并导致卵巢早衰。我们的研究证明了 PRC1 介导的基因沉默在女性生殖寿命中的基本作用,

更新日期:2022-08-10
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