The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Roles of E. coli DNA polymerases IV and V in lesion-targeted and untargeted SOS mutagenesis
Abstract
The expression of the Escherichia coli DNA polymerases pol V (UmuD'2C complex) and pol IV (DinB) increases in response to DNA damage. The induction of pol V is accompanied by a substantial increase in mutations targeted at DNA template lesions in a process called SOS-induced error-prone repair. Here we show that the common DNA template lesions, TT (6-4) photoproducts, TT cis-syn photodimers and abasic sites, are efficiently bypassed within 30 seconds by pol V in the presence of activated RecA protein (RecA*), single-stranded binding protein (SSB) and pol III's processivity beta,gamma-complex. There is no detectable bypass by either pol IV or pol III on this time scale. A mutagenic 'signature' for pol V is its incorporation of guanine opposite the 3'-thymine of a TT (6-4) photoproduct, in agreement with mutational spectra. In contrast, pol III and pol IV incorporate adenine almost exclusively. When copying undamaged DNA, pol V exhibits low fidelity with error rates of around 10(-3) to 10(-4), with pol IV being 5- to 10-fold more accurate. The effects of RecA protein on pol V, and beta,gamma-complex on pol IV, cause a 15,000- and 3,000-fold increase in DNA synthesis efficiency, respectively. However, both polymerases exhibit low processivity, adding 6 to 8 nucleotides before dissociating. Lesion bypass by pol V does not require beta,gamma-complex in the presence of non-hydrolysable ATPgammaS, indicating that an intact RecA filament may be required for translesion synthesis.
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“These multiplet mutations are likely the consequence of error-prone bypass polymerization during translesion synthesis and are consistent with the processivity of bypass polymerases persisting for several nucleotides after the bypass-requiring blocking lesion (39 -41).”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [41]
Citations
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Metadata
- Authors
- Tang, M., Pham, P., Shen, X., Taylor, J.-S., O'Donnell, M., Woodgate, R., & Goodman, M. F.
- Affiliations
- University of Southern California (US)
- Washington University in St. Louis (US)
- National Institutes of Health (US)
- Corresponding author
- Goodman, Myron F.
- Venue
- Nature
- Published
- 2000-04
- Volume
- 404
- Issue
- 6781
- Pages
- 1014-1018
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1510371408
- Cited by
- 443
- References
- 30
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 6 · 2023: 5 · 2022: 7 · 2021: 5 · 2020: 9 · 2019: 6 · 2018: 12 · 2017: 14 · 2016: 10 · 2015: 10 · 2014: 19 · 2013: 13 · 2012: 21
- FWCI
- 16.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- DNA polymerase IV, DNA polymerase V, DinB, SOS response, error-prone DNA repair, translesion synthesis, 6-4 photoproducts, abasic sites, RecA filament, polymerase fidelity, mutational signatures, DNA damage response
- MeSH terms
- DNA Damage, DNA-Directed DNA Polymerase, DNA, Bacterial, Escherichia coli, Rec A Recombinases, SOS Response, Genetics, Templates, Genetic, Mutagenesis, DNA Polymerase beta, Escherichia coli Proteins
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