精原干细胞（SSCs）基因组稳定性与男性不育密切相关，但具体机制不明。REV7是新发现能够通过构建Shieldin复合物调控DNA损伤非同源重组修复（NHEJ）通路中的重要因子，但在SSCs中具体作用未知。我们前期测序结果提示REV7基因在临床不育男性SSCs中差异表达；且Rev7条件敲除的雄性动物具有明确不育表型；通过质谱分析提示REV7能在SSCs NHEJ修复途径中发挥作用，故进一步探究REV7影响SSCs基因组稳定性机制对男性不育诊治有重要意义。本研究拟以Rev7过表达及敲降精原干细胞系及条件性敲除的小鼠为模型，结合ChIP-seq和SSCs移植等技术，探究REV7在维持SSCs基因组稳定性方面的作用，解析REV7能够介导Shieldin复合物调控SSCs DNA损伤修复通路的相关机制，并进一步验证REV7对SSCs生精能力的影响。其结果有望为临床男性不育的诊治提供新的思路和见解。

Genomic stability of spermatogonial stem cells (SSCs) is closely related to male infertility, but the mechanism is unclear. REV7, a newly discovered subunit of Shieldin complex, regulates non homologous end join (NHEJ) reapir pathway in DNA damage response, but its specific role in SSCs still remains unknown. Our previous experiments demonstrated that Rev7 gene was down regulated in SSCs from clinical male infertility patients, and there was an obvious sterile phenotype in testes from Rev7 conditional knockout animals. It was implied that REV7 might combine with crucial proteins in NHEJ pathway via mass spectrometry. Thus, further exploring the mechanism of REV7 in maintaining genome stability will facilitate male infertility clinical treatment. In present research, Rev7 overexpression/knockdown SSCs and conditional knockout mice will be applied to study the role of REV7 in maintaining the genome stability. The mechanism of REV7 in DNA damage repair pathway will be studied via ChIP-seq and SSCs transplantation techniques, and the effect of REV7 on SSCs biological functions will be further verified. Results are expected to provide new insights into clinical diagnosis and treatment of male infertility.