期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 106, 期 31, 页码 12765-12770出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0904623106
关键词
checkpoint; DNA damage; S phase; replication stress response
资金
- Howard Hughes Medical Institute Funding Source: Medline
- NIGMS NIH HHS [5 T32 GM07196-30, 2 T32 GM07196-29, T32 GM007196] Funding Source: Medline
DNA replication stress activates a response pathway that stabilizes stalled forks and promotes the completion of replication. The budding yeast Mec1 sensor kinase, Mrc1 mediator, and Rad53 effector kinase are central to this signal transduction cascade in S phase. We report that Mec1-dependent, Rad53-independent phosphorylation of Mrc1 is required to establish a positive feedback loop that stabilizes Mec1 and the replisome at stalled forks. A structure-function analysis of Mrc1 also uncovered a central region required for proper mediator function and association with replisome components. Together these results reveal new insight into how Mrc1 facilitates checkpoint signal amplification at stalled replication forks.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据