Altered translesion synthesis in E. coli Pol V mutants selected for increased recombination inhibition

Sommer, Suzanne, Becherel, Olivier J., Coste, Geneviève, Bailone, Adriana and Fuchs, Robert P. P. (2003) Altered translesion synthesis in E. coli Pol V mutants selected for increased recombination inhibition. DNA Repair, 2 12: 1361-1369. doi:10.1016/j.dnarep.2003.08.008


Author Sommer, Suzanne
Becherel, Olivier J.
Coste, Geneviève
Bailone, Adriana
Fuchs, Robert P. P.
Title Altered translesion synthesis in E. coli Pol V mutants selected for increased recombination inhibition
Formatted title
Altered translesion synthesis in E. coli Pol V mutants selected for increased recombination inhibition
Journal name DNA Repair   Check publisher's open access policy
ISSN 1568-7864
1568-7856
Publication date 2003-12-09
Sub-type Article (original research)
DOI 10.1016/j.dnarep.2003.08.008
Open Access Status Not yet assessed
Volume 2
Issue 12
Start page 1361
End page 1369
Total pages 9
Place of publication Amsterdam, Netherlands
Publisher Elsevier BV
Language eng
Formatted abstract
Replication of damaged DNA, also termed as translesion synthesis (TLS), involves specialized DNA polymerases that bypass DNA lesions. In Escherichia coli, although TLS can involve one or a combination of DNA polymerases depending on the nature of the lesion, it generally requires the Pol V DNA polymerase (formed by two SOS proteins, UmuD′ and UmuC) and the RecA protein. In addition to being an essential component of translesion DNA synthesis, Pol V is also an antagonist of RecA-mediated recombination. We have recently isolated umuD′ and umuC mutants on the basis of their increased capacity to inhibit homologous recombination. Despite the capacity of these mutants to form a Pol V complex and to interact with the RecA polymer, most of them exhibit a defect in TLS. Here, we further characterize the TLS activity of these Pol V mutants in vivo by measuring the extent of error-free and mutagenic bypass at a single (6-4)TT lesion located in double stranded plasmid DNA. TLS is markedly decreased in most Pol V mutants that we analyzed (8/9) with the exception of one UmuC mutant (F287L) that exhibits wild-type bypass activity. Somewhat unexpectedly, Pol V mutants that are partially deficient in TLS are more severely affected in mutagenic bypass compared to error-free synthesis. The defect in bypass activity of the Pol V mutant polymerases is discussed in light of the location of the respective mutations in the 3D structure of UmuD′ and the DinB/UmuC homologous protein Dpo4 of Sulfolobus solfataricus.
Keyword Bypass polymerase
E. coli Pol V DNA polymerase
SOS mutagenesis
Translesion synthesis
UV-induced base substitution mutagenesis
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Centre for Clinical Research Publications
 
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Created: Tue, 09 Aug 2016, 16:17:37 EST by Olivier Becherel on behalf of Learning and Research Services (UQ Library)