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Cited by 27DNA Repair MechanismsBacterial Genetics and BiotechnologyGenetic factors in colorectal cancer

Suppressors of Escherichia coli mutT: antimutators for DNA replication errors

Schaaper, Roel M.·1996·Mutation research. Fundamental and molecular mechanisms of mutagenesis
DOI 10.1016/0027-5107(95)00086-0
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Abstract

Previous studies in our laboratory used a papillation assay to identify a set of mutations in the E. coli dnaE gene that confer increased accuracy of DNA replication (antimutators). These antimutators were isolated as suppressors of the hugh mutability of a mismatch-repair-defective mutL strain, in which the majority of mutations represent uncorrected replication errors (mainly A.T --> G.C and G.C --> A.T transitions). In the present study, we have sought suppressors of the high mutability of a mutT mutator strain. mutT strains produce a high frequency of A.T --> C.G transversions due to their lack of the mutT-encoded 8-oxo-dGTPase, leading to a high frequency of A.(8-oxoG) mispairing errors. Following localized mutagenesis of the dnaE-dnaQ region of the chromosome, two strong suppressors of mutT mutability were obtained, both residing in the dnaE gene (dnaE940 and dnaE941). When subsequently tested in a mutL strain, these two alleles also proved antimutators in this background, dnaE941 being significantly stronger than the previously isolated antimutators. The results suggest that the DNA polymerase may use similar mechanisms to discriminate against A.(8-oxoG) transversion mispairs and A.C or T.G transition mispairs. The finding may also have significance for teh interpretation of the antimutator effect conferred by these dnaE alleles in a wild-type (mut+) background.

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  • These alleles also reduce specific transition mutations, making it unclear whether replication errors in wild-type cells stem from the intrinsic fidelity of DNA polymerase III or specific subpopulations with unique properties.

    “However, these alleles also reduce specific transition mutations, making it unclear whether replication errors in wild-type cells stem from the intrinsic fidelity of DNA polymerase III or specific subpopulations with unique properties [77].”

    From DNA Data Storage. (2023) · cites this paper as [77]

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Authors
Schaaper, R. M.
Affiliations
National Institutes of Health (US)
Corresponding author
Schaaper, Roel M.
ORCID
Schaaper, Roel M.
Venue
Mutation research. Fundamental and molecular mechanisms of mutagenesis
Publisher
Elsevier BV
Published
1996-02
Volume
350
Issue
1
Pages
17-23
ISSN
  • 0027-5107 (ISSN-L)
  • 1386-1964
DOI
10.1016/0027-5107(95)00086-0
OpenAlex
W2007411058
Cited by
27
References
18
Citations by year
2025: 2 · 2023: 1 · 2022: 1 · 2021: 1 · 2019: 1 · 2018: 2 · 2017: 1 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
0.63
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
  • PubMed (publishedVersion)
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
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
Keywords
MutT, DNA replication fidelity, 8-oxoguanine, DNA polymerase, dnaE, suppressors, MutL, DNA mismatch repair, transversions, transition, mispairing, Escherichia coli
MeSH terms
8-Hydroxy-2'-Deoxyguanosine, Alleles, Bacterial Proteins, Chromosomes, Bacterial, Deoxyguanosine, DNA Repair, DNA Replication, Escherichia coli, Genetic Markers, Genotype, Phenotype, Phosphoric Monoester Hydrolases, Pyrophosphatases, Suppression, Genetic, Mutagenesis, Escherichia coli Proteins, DNA Repair Enzymes

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