DNA damage in oocytes can cause infertility and birthdefects. DNA double-strand breaks (DSBs) are highlydeleterious and can substantially impair genomeintegrity. Homologous recombination (HR)-mediatedDNA DSB repair plays dominant roles in safeguardingoocyte quantity and quality. However, little is knownregarding the key players of the HR repair pathwayin oocytes. Here, we identified oocyte-specific geneOoep as a novel key component of the HR repairpathway in mouse oocytes. OOEP was required forefficient ataxia telangiectasia mutated (ATM) kinaseactivation and Rad51 recombinase (RAD51) focalaccumulation at DNA DSBs. Ooep null oocytes weredefective in DNA DSB repair and prone to apoptosisupon exogenous DNA damage insults. Moreover, Ooepnull oocytes exhibited delayed meiotic maturation.Therefore, OOEP played roles in preserving oocytequantity and quality by maintaining genome stability.Ooep expression decreased with the advance ofmaternal age, suggesting its involvement in maternalaging.