{"doi":"10.1128/jb.180.13.3345-3352.1998","title":"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\n            <i>Escherichia coli</i>","abstract":"<jats:title>ABSTRACT</jats:title>\n          <jats:p>\n            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\n            <jats:italic>Escherichia coli</jats:italic>\n            , 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.\n          </jats:p>","journal":"Journal of Bacteriology","year":1998,"id":36101,"datarank":4.137604805797048,"base_score":4.59511985013459,"endowment":4.59511985013459,"self_citation_contribution":0.6892679775201885,"citation_network_contribution":3.4483368282768594,"self_endowment_contribution":0.6892679775201885,"citer_contribution":3.4483368282768594,"corpus_percentile":null,"corpus_rank":null,"citation_count":98,"citer_count":77,"citers_with_citation_signal":73,"citers_with_endowment":73,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":48.75,"fair_percentile":44.94283201407212,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":183521,"name":"Philip C. Hanawalt","orcid":null,"position":1,"is_corresponding":false},{"id":183520,"name":"David J. Crowley","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":4.59511985013459,"endowment":4.59511985013459,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"9642186","pmcid":"PMC107288","openalex_id":"https://openalex.org/W2130441748","authors":[],"funders":[{"funder_name":"NIGMS NIH HHS","grant_id":"GM07276","title":null},{"funder_name":"NIGMS NIH HHS","grant_id":"T32 GM007276","title":null},{"funder_name":"NCI NIH HHS","grant_id":"CA44349","title":null}],"total_grants":3,"fwci":2.5322,"citation_percentile":0.9021682,"influential_citations":11,"citation_trend":[{"year":2012,"count":6},{"year":2013,"count":1},{"year":2014,"count":7},{"year":2015,"count":3},{"year":2017,"count":3},{"year":2019,"count":1},{"year":2020,"count":3},{"year":2021,"count":4},{"year":2022,"count":3},{"year":2023,"count":3},{"year":2024,"count":2},{"year":2025,"count":2},{"year":2026,"count":1}],"oa_status":"bronze","license":"https://journals.asm.org/non-commercial-tdm-license","oa_locations":[{"url":"https://jb.asm.org/content/jb/180/13/3345.full.pdf","host_type":"journal"},{"url":"https://jb.asm.org/content/jb/180/13/3345.full.pdf","host_type":"BRONZE"},{"url":"https://jb.asm.org/content/jb/180/13/3345.full.pdf","host_type":"publisher"},{"url":"https://journals.asm.org/doi/pdf/10.1128/JB.180.13.3345-3352.1998","host_type":"publisher"},{"url":"https://doi.org/10.1128/jb.180.13.3345-3352.1998","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9642186","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/107288","host_type":"repository"},{"url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC107288/pdf/jb003345.pdf","host_type":"repository"}],"fields_of_study":["DNA Repair Mechanisms","CRISPR and Genetic Engineering","DNA and Nucleic Acid Chemistry","Biology","Medicine","Chemistry","Environmental Science","Adenosine Triphosphatases","Bacterial Proteins","DNA Damage","DNA Helicases","DNA Repair","DNA-Binding Proteins","Escherichia coli","Escherichia coli Proteins","Kinetics","Pyrimidine Dimers","Rifampin","SOS Response, Genetics","Time Factors","Transcription, Genetic","Ultraviolet Rays"],"mesh_terms":["Adenosine Triphosphatases","Bacterial Proteins","DNA Damage","DNA Repair","DNA Helicases","DNA-Binding Proteins","Escherichia coli","Kinetics","Pyrimidine Dimers","Rifampin","SOS Response, Genetics","Time Factors","Transcription, Genetic","Ultraviolet Rays","Escherichia coli Proteins"],"keywords":["Pyrimidine dimer","Nucleotide excision repair","Biology","SOS response","DNA repair","DNA damage","Escherichia coli","Mutant","Transcription (linguistics)","DNA","Molecular biology","Cell 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