ArticleJournal of bacteriology2002
Escherichia coli DNA polymerase III can replicate efficiently past a T-T cis-syn cyclobutane dimer if DNA polymerase V and the 3' to 5' exonuclease proofreading function encoded by dnaQ are inactivated.
Article in Journal of bacteriology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Replisome-mediated translesion synthesis by a cellular replicase.The Journal of biological chemistry · 2017Article
- DNA Replication in Mycobacterium tuberculosis.Microbiology spectrum · 2017Review
- Interactions and Localization of Escherichia coli Error-Prone DNA Polymerase IV after DNA Damage.Journal of bacteriology · 2015Article
- Regulation of Mutagenic DNA Polymerase V Activation in Space and Time.PLoS genetics · 2015Article
- Translesion DNA Synthesis.EcoSal Plus · 2012Article
- Simple and efficient purification of Escherichia coli DNA polymerase V: cofactor requirements for optimal activity and processivity in vitro.DNA repair · 2012Article
- Mechanisms employed by Escherichia coli to prevent ribonucleotide incorporation into genomic DNA by Pol V.PLoS genetics · 2012Article
- The role of Fpg protein in UVC-induced DNA lesions.Redox report : communications in free radical research · 2012Article
- Increase in dNTP pool size during the DNA damage response plays a key role in spontaneous and induced-mutagenesis in Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Mutagenicity induced by UVC in Escherichia coli cells: reactive oxygen species involvement.Redox report : communications in free radical research · 2011Article
- Essential roles for imuA'- and imuB-encoded accessory factors in DnaE2-dependent mutagenesis in Mycobacterium tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Steric gate variants of UmuC confer UV hypersensitivity on Escherichia coli.Journal of bacteriology · 2009Article
- DNA polymerase switching: effects on spontaneous mutagenesis in Escherichia coli.Molecular microbiology · 2009Article
- Biological properties of single chemical-DNA adducts: a twenty year perspective.Chemical research in toxicology · 2008Review
- The Escherichia coli histone-like protein HU has a role in stationary phase adaptive mutation.Genetics · 2007Article
- Accessory proteins assist exonuclease-deficient bacteriophage T4 DNA polymerase in replicating past an abasic site.The Biochemical journal · 2007Article
- Involvement of Y-family DNA polymerases in mutagenesis caused by oxidized nucleotides in Escherichia coli.Journal of bacteriology · 2006Article
- Article
- Recruitment of host functions suggests a repair pathway for late steps in group II intron retrohoming.Genes & development · 2005Article
- Error-prone DNA polymerase IV is regulated by the heat shock chaperone GroE in Escherichia coli.Journal of bacteriology · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Although very little replication past a T-T cis-syn cyclobutane dimer normally takes place in Escherichia coli in the absence of DNA polymerase V (Pol V), we previously observed as much as half of the wild-type bypass frequency in Pol V-deficient (DeltaumuDC) strains if the 3' to 5' exonuclease proofreading activity of the Pol III epsilon subunit was also disabled by mutD5. This observation might be explained in at least two ways. In the absence of Pol V, wild-type Pol III might bind preferentially to the blocked primer terminus but be incapable of bypass, whereas the proofreading-deficient enzyme might dissociate more readily, providing access to bypass polymerases. Alternatively, even though wild-type Pol III is generally regarded as being incapable of lesion bypass, proofreading-impaired Pol III might itself perform this function. We have investigated this issue by examining dimer bypass frequencies in DeltaumuDC mutD5 strains that were also deficient for Pol I, Pol II, and Pol IV, both singly and in all combinations. Dimer bypass frequencies were not decreased in any of these strains and indeed in some were increased to levels approaching those found in strains containing Pol V. Efficient dimer bypass was, however, entirely dependent on the proofreading deficiency imparted by mutD5, indicating the surprising conclusion that bypass was probably performed by the mutD5 Pol III enzyme itself. This mutant polymerase does not replicate past the much more distorted T-T (6-4) photoadduct, however, suggesting that it may only replicate past lesions, like the T-T dimer, that form base pairs normally.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.