ArticleProceedings of the National Academy of Sciences of the United States of America2014
Stalled transcription complexes promote DNA repair at a distance.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- Structural basis for loading of transcription repair-coupling factor Mfd onto stalled elongation complexes.Nucleic acids research · 2026Article
- RNAP-seq:bioRxiv : the preprint server for biology · 2026Article
- Structural basis for loading of Transcription Repair-Coupling factor Mfd onto stalled elongation complexes.bioRxiv : the preprint server for biology · 2025Article
- Mfd deficiency decreases the abundance of complete transcripts of sporulation genes and alters sporogenesis and the structure of dormantFrontiers in microbiology · 2025Article
- Isolation of E. coli RNA polymerase transcription elongation complexes by selective solid-phase photoreversible immobilization.Methods in enzymology · 2023Article
- Mechanism of transcription modulation by the transcription-repair coupling factor.Nucleic acids research · 2022Article
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Single-molecule studies of helicases and translocases in prokaryotic genome-maintenance pathways.DNA repair · 2021Review
- Mfd - at the crossroads of bacterial DNA repair, transcriptional regulation and molecular evolvability.Transcription · 2021Review
- Article
- A Peek Inside the Machines of Bacterial Nucleotide Excision Repair.International journal of molecular sciences · 2021Review
- Mfd Affects Global Transcription and the Physiology of StressedFrontiers in microbiology · 2021Article
- Molecular determinants for dsDNA translocation by the transcription-repair coupling and evolvability factor Mfd.Nature communications · 2020Article
- Single-molecule imaging reveals molecular coupling between transcription and DNA repair machinery in live cells.Nature communications · 2020Article
- Gre-family factors modulate DNA damage sensing byRNA biology · 2019Article
- Transcription of Bacterial Chromatin.Journal of molecular biology · 2019Review
- Mfd protects against oxidative stress in Bacillus subtilis independently of its canonical function in DNA repair.BMC microbiology · 2019Article
- Recruitment of UvrBC complexes to UV-induced damage in the absence of UvrA increases cell survival.Nucleic acids research · 2018Article
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4 authors at 1 institution in 1 country.
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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 polarity suppressor) transcription pause site, which causes backtracking of RNAP, can promote the repair of downstream lesions when those lesions do not themselves cause the polymerase to stall. Our findings indicate that the transcription-repair coupling factor Mfd, which is an ATP-dependent superfamily 2 helicase that binds to RNAP, continues to translocate along DNA after RNAP has been displaced until a lesion in the template strand is located. The discovery that pause sites can promote the repair of nonstalling lesions suggests that TCR pathways may play a wider role in modulating mutation frequencies in different parts of the genome than has previously been suspected.
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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.