期刊
NATURE
卷 490, 期 7420, 页码 431-434出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nature11430
关键词
-
资金
- Frontieres Interdisciplinaires du Vivant Doctoral Program
- Fondation pour la Recherche Medicale
- BBSRC [BB/I003142/1]
- National Institutes of Health [GM073829]
- EURYI grant
- CNRS
- University of Paris Diderot
- Biotechnology and Biological Sciences Research Council [BB/I003142/1, BB/I001859/1] Funding Source: researchfish
- BBSRC [BB/I001859/1, BB/I003142/1] Funding Source: UKRI
Transcription-coupled DNA repair uses components of the transcription machinery to identify DNA lesions and initiate their repair. These repair pathways are complex, so their mechanistic features remain poorly understood. Bacterial transcription-coupled repair is initiated when RNA polymerase stalled at a DNA lesion is removed by Mfd, an ATP-dependent DNA translocase(1-3). Here we use single-molecule DNA nanomanipulation to observe the dynamic interactions of Escherichia coli Mfd with RNA polymerase elongation complexes stalled by a cyclopyrimidine dimer or by nucleotide starvation. We show that Mfd acts by catalysing two irreversible, ATP-dependent transitions with different structural, kinetic and mechanistic features. Mfd remains bound to the DNA in a long-lived complex that could act as a marker for sites of DNA damage, directing assembly of subsequent DNA repair factors. These results provide a framework for considering the kinetics of transcription-coupled repair in vivo, and open the way to reconstruction of complete DNA repair pathways at single-molecule resolution.
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