DNA修复是维持生物体基因组稳定的直接有效方式。DNA修复异常会导致基因组不稳定（基因重排、染色体丢失、融合或移码等）、细胞死亡以及包括癌症在内的多种遗传性疾病的发生。同源重组修复（homologous recombination，HR）是高保真的修复方式，主要发生在S/G2期。由MRN和CtIP参与的DNA末端切割是HR修复的第一步。DNA末端切割产生的3’ssDNA突出末端通过招募单链DNA结合蛋白到DNA损伤位点促进同源重组修复。在真核生物中，SOSS及RPA是参与DNA损伤修复的主要单链DNA结合蛋白。本课题拟利用前期工作中对SOSS及HR修复的研究基础，对SOSS及RPA促进HR修复的分子机制及其调控过程进行深入研究，从而阐明SOSS和RPA的这两种单链DNA结合蛋白之间的关系及其在HR修复过程中的作用机制。研究结果有望为HR修复缺陷相关疾病的诊断和治疗提供理论基础。

DNA repair maintains the stability and integrity of genomic DNA. Unrepaired or incorrectly repaired DNA damage can cause genome instability (such as gene rearrangement, chromosome loss, gene fusion or frame shift), cell death and promote the genesis of genetic disease including tumor. Homologous recombination (HR) is an error-free DSBs (Double strand breaks) repair pathway, which is active mainly in S and G2 phases of the cell cycle. DNA end resection initiated by the MRN (MRE11, RAD50, and NBS1) complex and CtIP, is the initial step of HR and generates 3′overhang ssDNA tails that are first coated by single-strand binding proteins (SSBs). In eukaryotes, SOSS (sensor of ssDNA) complex and RPA complex are the main SSBs involved in the repair of damaged DNA. This work aims to illuminate the relationship between SOSS and RPA complex and supplement the molecular mechanism of HR repair. The results obtained in this study will provide a theoretical basis for the diagnosis and cure of HR related diseases.