{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Haines NM"],"funding":["Biotechnology and Biological Sciences Research Council"],"pagination":["4037-42"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3964087"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["111(11)"],"pubmed_abstract":["Transcription-coupled nucleotide excision repair (TCR) accelerates the removal of noncoding lesions from the template strand of active genes, and hence contributes to genome-wide variations in mutation frequency. Current models for TCR suppose that a lesion must cause RNA polymerase (RNAP) to stall if it is to be a substrate for accelerated repair. We have examined the substrate requirements for TCR using a system in which transcription stalling and damage location can be uncoupled. We show that Mfd-dependent TCR in bacteria involves the formation of a damage search complex that can detect lesions downstream of a stalled RNAP, and that the strand specificity of the accelerated repair pathway is independent of the requirement for a lesion to stall RNAP. We also show that an ops (operon pola"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Stalled transcription complexes promote DNA repair at a distance."],"pmcid":["PMC3964087"],"funding_grant_id":["BB/I001859/1","1095379","BB/I003142/1"],"pubmed_authors":["Savery NJ","Kim YI","Haines NM","Smith AJ"],"additional_accession":[]},"is_claimable":false,"name":"Stalled transcription complexes promote DNA repair at a distance.","description":"Transcription-coupled nucleotide excision repair (TCR) accelerates the removal of noncoding lesions from the template strand of active genes, and hence contributes to genome-wide variations in mutation frequency. Current models for TCR suppose that a lesion must cause RNA polymerase (RNAP) to stall if it is to be a substrate for accelerated repair. We have examined the substrate requirements for TCR using a system in which transcription stalling and damage location can be uncoupled. We show that Mfd-dependent TCR in bacteria involves the formation of a damage search complex that can detect lesions downstream of a stalled RNAP, and that the strand specificity of the accelerated repair pathway is independent of the requirement for a lesion to stall RNAP. We also show that an ops (operon pola","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Mar","modification":"2025-04-04T19:08:45.443Z","creation":"2019-03-27T01:23:52Z"},"accession":"S-EPMC3964087","cross_references":{"pubmed":["24554077"],"doi":["10.1073/pnas.1322350111"]}}