Regulation of Double Strand Break Repair

双链断裂修复的调控

• 批准号: 7204220
• 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/7204220
• 关键词: Address; C-terminal; Cell Cycle; Cells; DNA Damage; DNA Double Strand Break; DNA biosynthesis; DNA lesion; Dependency; Diffuse; Double Strand Break Repair; Event; Frequencies; Genetic Recombination; Goals; Histone H2A; Imagery; Mediating; Methods; Mutation; Nuclear; Personal Satisfaction; Phase; Phosphorylation; Phosphotransferases; Play; Proteins; Rad52 protein; Regulation; Relative (related person); Replication Initiation; Role; Saccharomyces cerevisiae; Time; in vivo; repaired; response

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)：针对导致双链断裂的脱氧核糖核酸损伤，重组蛋白Rad52在脱氧核糖核酸复制启动和S时相进入后形成离散的核病灶。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的依赖来阐明RAD52焦点形成的控制和时机选择的潜在机制。此外，还提出了一种体内可视化的方法，用于显示DNA损伤后的磷酸化事件，特别是组蛋白H2A的磷酸化事件。最后，在酿酒酵母H_2A中分离出对DNA损伤敏感的突变。将分析这些突变对体内DSB的识别和修复的影响。