論文

査読有り
2015年2月

Recombinase and translesion DNA polymerase decrease the speed of replication fork progression during the DNA damage response in Escherichia coli cells

NUCLEIC ACIDS RESEARCH
  • Kang Wei Tan
  • ,
  • Tuan Minh Pham
  • ,
  • Asako Furukohri
  • ,
  • Hisaji Maki
  • ,
  • Masahiro Tatsumi Akiyama

43
3
開始ページ
1714
終了ページ
1725
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1093/nar/gkv044
出版者・発行元
OXFORD UNIV PRESS

The SOS response is a DNA damage response pathway that serves as a general safeguard of genome integrity in bacteria. Extensive studies of the SOS response in Escherichia coli have contributed to establishing the key concepts of cellular responses to DNA damage. However, how the SOS response impacts on the dynamics of DNA replication fork movement remains unknown. We found that inducing the SOS response decreases the mean speed of individual replication forks by 30-50% in E. coli cells, leading to a 20-30% reduction in overall DNA synthesis. dinB and recA belong to a group of genes that are upregulated during the SOS response, and encode the highly conserved proteins DinB (also known as DNA polymerase IV) and RecA, which, respectively, specializes in translesion DNA synthesis and functions as the central recombination protein. Both genes were independently responsible for the SOS-dependent slowdown of replication fork progression. Furthermore, fork speed was reduced when each gene was ectopically expressed in SOS-uninduced cells to the levels at which they are expressed in SOS-induced cells. These results clearly indicate that the increased expression of dinB and recA performs a novel role in restraining the progression of an unperturbed replication fork during the SOS response.

リンク情報
DOI
https://doi.org/10.1093/nar/gkv044
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25628359
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000351638000038&DestApp=WOS_CPL
ID情報
  • DOI : 10.1093/nar/gkv044
  • ISSN : 0305-1048
  • eISSN : 1362-4962
  • PubMed ID : 25628359
  • Web of Science ID : WOS:000351638000038

エクスポート
BibTeX RIS