Regulation of Double Strand Break Repair

描述（由申请人提供）：为了应对DNA损伤导致的双链断裂（DSBs），重组蛋白Rad52在DNA复制开始和S期进入后形成离散的核灶。本项目的目标是通过解决DSB修复（DSBR）对DNA复制或细胞周期调节因子的依赖性，阐明Rad52焦点形成的控制和定时机制。此外，提出了一种体内可视化磷酸化事件的方法，特别是组蛋白H2A响应DNA损伤的方法。最后，分离出酿酒链球菌H2A对DNA损伤敏感的突变。我们将分析这些突变对dsb在体内的识别和修复的影响。

DESCRIPTION (provided by applicant): In response to DNA damage causing double strand breaks (DSBs), the recombination protein Rad52 forms discrete nuclear foci after the initiation of DNA replication and S phase entry. The goal of this project is to elucidate the mechanisms underlying the control and timing of Rad52 focus formation by addressing the dependency of DSB repair (DSBR) on DNA replication or cell cycle regulators. Additionally, a method for in vivo visualization of phosphorylation events, particularly that of histone H2A in response to DNA damage is proposed. Finally, mutations in S. cerevisiae H2A conferring sensitivity to DNA damage have been isolated. These mutations will be analyzed for their effect on both the recognition and the repair of DSBs in vivo.