Maternal gene Ooep may participate in homologous recombination-mediated DNA double-strand break repair in mouse oocytes

• Published in: Dōngwùxué yánjiū Vol. 39; no. 6; pp. 387 - 395
• Main Authors: He, Da-Jian, Wang, Lin, Zhang, Zhi-Bi, Guo, Kun, Li, Jing-Zheng, He, Xie-Chao, Cui, Qing-Hua, Zheng, Ping
• Format: Journal Article
• Language: English
• Published: China Kunming Institute of Zoology, The Chinese Academy of Sciences 18.11.2018
• Subjects: Ageing; Aging; Apoptosis; Ataxia; Ataxia telangiectasia mutated protein; Birth defects; Cells; Congenital defects; Defects; Deoxyribonucleic acid; DNA; DNA damage; DNA repair; Double-strand break repair; Gene expression; Genes; Genomes; Homologous recombination; Homology; Infertility; Meiosis; Oocytes; Recombinase; Recombination; Repair; Rodents; Stability; United States > US; Germany
• ISSN: 2095-8137; 0254-5853
• DOI: 10.24272/j.issn.2095-8137.2018.067

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.