Cited by 443DNA Repair MechanismsBacterial Genetics and BiotechnologyCarcinogens and Genotoxicity Assessment

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Roles of E. coli DNA polymerases IV and V in lesion-targeted and untargeted SOS mutagenesis

Tang, Mengjia, Pham, Phuong, Shen, Xuan, Taylor, John-Stephen, O'Donnell, Mike, Woodgate, Roger, Goodman, Myron F.·2000·Nature

DOI 10.1038/35010020

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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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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.
ORCID: Tang, Mengjia
Pham, Phuong
Shen, Xuan
Taylor, John-Stephen
Woodgate, Roger
Goodman, Myron F.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2000-04
Volume: 404
Issue: 6781
Pages: 1014-1018
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/35010020
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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Roles of E. coli DNA polymerases IV and V in lesion-targeted and untargeted SOS mutagenesis

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