ArticlePLoS genetics2017
Processing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Genome-wide maps of UV damage repair and mutation suppression by CPD photolyase.Nucleic acids research · 2025Article
- Oxidative stress drives mutagenesis through transcription-coupled repair in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Bacterial DNA excision repair pathways.Nature reviews. Microbiology · 2022Review
- Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- A Comprehensive View of Translesion Synthesis in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2020Review
- Directed evolution of Escherichia coli with lower-than-natural plasmid mutation rates.Nucleic acids research · 2018Article
- Aberrant repair initiated by the adenine-DNA glycosylase does not play a role in UV-induced mutagenesis inPeerJ · 2018Article
- Illuminating genome repair by photolyase.Photochemistry and photobiologyArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally assumed that most point mutations are fixed when damage containing template DNA undergoes replication, either right at the fork or behind the fork during gap filling. Here we provide genetic evidence for a pathway, dependent on Nucleotide Excision Repair, that induces mutations when processing closely spaced lesions. This pathway, referred to as Nucleotide Excision Repair-induced Mutagenesis (NERiM), exhibits several characteristics distinct from mutations that occur within the course of replication: i) following UV irradiation, NER-induced mutations are fixed much more rapidly (t ½ ≈ 30 min) than replication dependent mutations (t ½ ≈ 80-100 min) ii) NERiM specifically requires DNA Pol IV in addition to Pol V iii) NERiM exhibits a two-hit dose-response curve that suggests processing of closely spaced lesions. A mathematical model let us define the geometry (infer the structure) of the toxic intermediate as being formed when NER incises a lesion that resides in close proximity of another lesion in the complementary strand. This critical NER intermediate requires Pol IV / Pol II for repair, it is either lethal if left unrepaired or mutation-prone when repaired. Finally, NERiM is found to operate in stationary phase cells providing an intriguing possibility for ongoing evolution in the absence of replication.
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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.