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（由申请人提供）：响应DNA损伤导致双链断裂（DSB），重组蛋白RAD52在启动DNA复制和S相进入后形成离散的核灶。该项目的目的是通过解决DSB修复（DSBR）对DNA复制或细胞周期调节剂的依赖性来阐明RAD52焦点形成的机制。此外，提出了一种磷酸化事件的体内可视化方法，尤其是组蛋白H2A响应DNA损伤的方法。最后，已经分离出对DNA损伤的敏感性的酿酒酵母中的突变。这些突变将分析它们对体内DSB的识别和修复的影响。