- THIS ARTICLE
- Full Text (Rapid PDF)
-
All Versions of this Article:
genetics.107.072405v1
176/3/1431 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Email this article to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Bjedov, I.
- Articles by Matic, I.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Bjedov, I.
- Articles by Matic, I.
doi:10.1534/genetics.107.072405
A more recent version of this article appeared on July 1, 2007.
REGULAR RESEARCH PAPERS |
Involvement of Escherichia coli DNA polymerase IV in tolerance of cytotoxic alkylating DNA lesions in vivo
Ivana Bjedov 1, Chitralekha Nag Dasgupta 1, Dea Slade 1, Sophie Le Blastier 1, Marjorie Selva 1 and Ivan Matic 1*
1 Faculté de Médecine, Université Paris 5
* To whom correspondence should be addressed. E-mail: matic{at}necker.fr.
Submitted on February 20, 2007
Revised on March 26, 2007
Accepted on 3 May 2007
Escherichia coli PolIV, a DNA polymerase capable to catalyze synthesis past replication-blocking DNA lesions, belongs to the most ubiquitous branch of Y-family DNA polymerases. The goal of this study is to identify spontaneous DNA damage that is bypassed specifically and accurately by PolIV in vivo. We increased the amount of spontaneous DNA lesions using mutants deficient for different DNA repair pathways and measured mutation frequency in PolIV proficient and deficient backgrounds. We found that PolIV performs error-free bypass of DNA damage that accumulates in the alkA tag genetic background. This result indicates that PolIV is involved in the error-free bypass of cytotoxic alkylating DNA lesions. When the amount cytotoxic alkylating DNA lesions is increased by the treatment with chemical alkylating agents, PolIV is required for survival in alkA tag proficient genetic background, as well. Our study, together with the reported involvement of mammalian PolIV homolog, Pol
, in similar activity, indicates that Y-family DNA polymerases from DinB branch can be added to the list of evolutionarily conserved molecular mechanisms that counteract cytotoxic effects of DNA alkylation. This activity is of major biological relevance because alkylating agents are continuously produced endogenously in all living cells and are also present in the environment.
Key Words: DNA repair, Escherichia coli, alkylation damage, dinB
This article has been cited by other articles:
![]() |
R. S. Galhardo, R. Do, M. Yamada, E. C. Friedberg, P. J. Hastings, T. Nohmi, and S. M. Rosenberg DinB Upregulation Is the Sole Role of the SOS Response in Stress-Induced Mutagenesis in Escherichia coli Genetics, May 1, 2009; 182(1): 55 - 68. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. S. Plosky, E. G. Frank, D. A. Berry, G. P. Vennall, J. P. McDonald, and R. Woodgate Eukaryotic Y-family polymerases bypass a 3-methyl-2'-deoxyadenosine analog in vitro and methyl methanesulfonate-induced DNA damage in vivo Nucleic Acids Res., April 1, 2008; 36(7): 2152 - 2162. [Abstract] [Full Text] [PDF] |
||||

