Oocytes are indispensable for mammalian life. Thus, it is important to understand how mature oocytes are generated. As a critical stage of oocytes development, meiosis has been extensively studied, yet how chromatin remodeling contributes to this process is largely unknown. Here, we demonstrate that the ATP-dependent chromatin remodeling factor Snf2h (also known as Smarca5) plays a critical role in regulating meiotic cell cycle progression. Females with oocyte-specific depletion of Snf2h are infertile and oocytes lacking Snf2h fail to undergo meiotic resumption. Mechanistically, depletion of Snf2h results in dysregulation of meiosis-related genes, which causes failure of maturation-promoting factor (MPF) activation. ATAC-seq analysis in oocytes revealed that Snf2h regulates transcription of key meiotic genes, such as Prkar2b, by increasing its promoter chromatin accessibility. Thus, our studies not only demonstrate the importance of Snf2h in oocyte meiotic resumption, but also reveal the mechanism underlying how a chromatin remodeling factor can regulate oocyte meiosis.

中文翻译：

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染色质重塑剂Snf2h对于卵母细胞减数分裂细胞周期进程至关重要。

卵母细胞是哺乳动物生活必不可少的。因此，重要的是要了解如何产生成熟的卵母细胞。作为卵母细胞发育的关键阶段，减数分裂已被广泛研究，但染色质重塑如何促成这一过程尚不清楚。在这里，我们证明了ATP依赖的染色质重塑因子Snf2h（也称为Smarca5）在调节减数分裂细胞周期进程中起着至关重要的作用。卵母细胞特异性消耗Snf2h的女性是不育的，缺乏Snf2h的卵母细胞无法减数分裂恢复。从机制上讲，Snf2h的消耗会导致减数分裂相关基因的失调，从而导致成熟促进因子（MPF）激活失败。卵母细胞中的ATAC-seq分析显示，Snf2h调节关键减数分裂基因（例如Prkar2b，通过增加其启动子染色质的可及性。因此，我们的研究不仅证明了Snf2h在卵母细胞减数分裂恢复中的重要性，而且揭示了染色质重塑因子如何调节卵母细胞减数分裂的潜在机制。