Regulation of Double Strand Break Repair

双链断裂修复的调控

• 批准号: 7035809
• 负责人: Jacqueline Barlow
• 金额: $ 3.27万
• 依托单位: COLUMBIA UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-01-01 至 2007-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7035809
• 关键词: DNA damage; DNA repair; Saccharomyces cerevisiae; cell growth regulation; fluorescence resonance energy transfer; genetic recombination; histones; phosphorylation; predoctoral investigator; recombinant proteins

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.

描述（申请人提供）：重组蛋白Rad52在DNA复制启动和进入S期后，响应DNA损伤引起的双链断裂（DSB），形成离散的核灶。本项目的目标是阐明的机制，通过解决DSB修复（DSBR）的依赖性DNA复制或细胞周期调节因子的Rad52焦点形成的控制和时间。此外，提出了一种用于磷酸化事件，特别是组蛋白H2A响应于DNA损伤的磷酸化事件的体内可视化的方法。最后，S.已分离出赋予对DNA损伤敏感性的酿酒酵母H2A。将分析这些突变对体内DSB识别和修复的影响。