DNA damage in oocytes can cause infertility and birth defects. DNA double-strand breaks (DSBs) are highly deleterious and can substantially impair genome integrity. Homologous recombination (HR)-mediated DNA DSB repair plays dominant roles in safeguarding oocyte quantity and quality. However, little is known regarding the key players of the HR repair pathway in oocytes. Here, we identified oocyte-specific gene Ooep as a novel key component of the HR repair pathway in mouse oocytes. OOEP was required for efficient ataxia telangiectasia mutated (ATM) kinase activation and Rad51 recombinase(RAD51)focal accumulation at DNA DSBs. Ooep null oocytes were defective in DNA DSB repair and prone to apoptosis upon exogenous DNA damage insults. Moreover, Ooep null oocytes exhibited delayed meiotic maturation. Therefore, OOEP played roles in preserving oocyte quantity and quality by maintaining genome stability. Ooep expression decreased with the advance of maternal age, suggesting its involvement in maternal aging.
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机译：卵母细胞的DNA损伤会导致不孕症和出生缺陷。 DNA双链休息（DSB）是高度有害的，可以显着损害基因组完整性。同源重组（HR）介导的DNA DNA DSB修复在保护卵母细胞的数量和质量方面发挥着主导作用。然而，关于卵母细胞中HR修复途径的关键玩家很少。在此，我们将卵母细胞特异性基因OOeP鉴定为小鼠卵母细胞中HR修复途径的新型关键组分。在DNA DSBS下，有效的Ataxia Telanciectasia突变（ATM）激酶激活和RAD51重组酶（RAD51）焦点积聚在DNA DNA DNAB中是必需的。 OOEP NULL OOCYTEs在DNA DNA修复中有缺陷，并且在外源DNA损伤时易于凋亡。此外，OOEP无效卵母细胞表现出延迟的减数分裂成熟。因此，OOEP通过维持基因组稳定性来保持卵母细胞量和质量的作用。 OOEP表达随着产妇年龄的进展而减少，表明其参与母体衰老。
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