ArticleJournal of bacteriology1998
Induction of the SOS response increases the efficiency of global nucleotide excision repair of cyclobutane pyrimidine dimers, but not 6-4 photoproducts, in UV-irradiated Escherichia coli.
Article in Journal of bacteriology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 98 citations in OpenAlex.
- Induced tolerance to UV stress drives survival heterogeneity in isogenic E. coli cell populations.Scientific reports · 2026Article
- Genome-wide strand-specific UV mutagenesis inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Induced tolerance to UV stress drives survival heterogeneity in isogenicbioRxiv : the preprint server for biology · 2025Article
- Dynamics of transcription-coupled repair of cyclobutane pyrimidine dimers and (6-4) photoproducts inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- In vitro DNA repair genomics using XR-seq withProceedings of the National Academy of Sciences of the United States of America · 2023Article
- A new technique for genome-wide mapping of nucleotide excision repair without immunopurification of damaged DNA.The Journal of biological chemistry · 2022Article
- Article
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
- Ultraviolet-induced RNA:DNA hybrids interfere with chromosomal DNA synthesis.Nucleic acids research · 2021Article
- Article
- Quantitative proteomic reveals gallium maltolate induces an iron-limited stress response and reduced quorum-sensing in Pseudomonas aeruginosa.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
- Single-molecule live-cell imaging visualizes parallel pathways of prokaryotic nucleotide excision repair.Nature communications · 2020Article
- Single-molecule imaging reveals molecular coupling between transcription and DNA repair machinery in live cells.Nature communications · 2020Article
- Recruitment of UvrBC complexes to UV-induced damage in the absence of UvrA increases cell survival.Nucleic acids research · 2018Article
- High-throughput identification and rational design of synergistic small-molecule pairs for combating and bypassing antibiotic resistance.PLoS biology · 2017Article
- Historical perspective on the DNA damage response.DNA repair · 2015Review
- UvrD helicase: an old dog with a new trick: how one step backward leads to many steps forward.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
- RNA polymerase between lesion bypass and DNA repair.Cellular and molecular life sciences : CMLS · 2013Review
- Inefficient replication reduces RecA-mediated repair of UV-damaged plasmids introduced into competent Escherichia coli.Plasmid · 2012Article
- Mfd is required for rapid recovery of transcription following UV-induced DNA damage but not oxidative DNA damage in Escherichia coli.Journal of bacteriology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nucleotide excision repair (NER) is responsible for the removal of a variety of lesions from damaged DNA and proceeds through two subpathways, global repair and transcription-coupled repair. In Escherichia coli, both subpathways require UvrA and UvrB, which are induced following DNA damage as part of the SOS response. We found that elimination of the SOS response either genetically or by treatment with the transcription inhibitor rifampin reduced the efficiency of global repair of the major UV-induced lesion, the cyclobutane pyrimidine dimer (CPD), but had no effect on the global repair of 6-4 photoproducts. Mutants in which the SOS response was constitutively derepressed repaired CPDs more rapidly than did wild-type cells, and this rate was not affected by rifampin. Transcription-coupled repair of CPDs occurred in the absence of SOS induction but was undetectable when the response was expressed constitutively. These results suggest that damage-inducible synthesis of UvrA and UvrB is necessary for efficient repair of CPDs and that the levels of these proteins determine the rate of NER of UV photoproducts. We compare our findings with recent data from eukaryotic systems and suggest that damage-inducible stress responses are generally critical for efficient global repair of certain types of genomic damage.
Indexed as
Identifiers
What OpenQuestion holds
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.