ArticleMolecular cell2012
Mechanism of translesion transcription by RNA polymerase II and its role in cellular resistance to DNA damage.
Article in Molecular cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 124 citations in OpenAlex.
- The hidden costs of imperfection: transcription errors in protein aggregation diseases.Current opinion in genetics & development · 2025Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- A cellular system to study responses to a collision between the transcription complex and a protein-bound nick in the DNA template.FEBS letters · 2025Article
- Synergistic effects of retinol and retinyl palmitate in alleviating UVB-induced DNA damage and promoting the homologous recombination repair in keratinocytes.Frontiers in pharmacology · 2025Article
- Replication-Independent ICL Repair: From Chemotherapy to Cell Homeostasis.Journal of molecular biology · 2024Review
- DNA lesion bypass and the stochastic dynamics of transcription-coupled repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Quantitative analysis of transcription start site selection reveals control by DNA sequence, RNA polymerase II activity and NTP levels.Nature structural & molecular biology · 2024Article
- Evolutionary conservation of the fidelity of transcription.Nature communications · 2023Article
- Effects of replication domains on genome-wide UV-induced DNA damage and repair.PLoS genetics · 2022Article
- Structural advances in transcription elongation.Current opinion in structural biology · 2022Review
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Photorepair of Either CPD or 6-4PP DNA Lesions in Basal Keratinocytes Attenuates Ultraviolet-Induced Skin Effects in Nucleotide Excision Repair Deficient Mice.Frontiers in immunology · 2022Article
- The emergence of the postgenomic gene.European journal for philosophy of science · 2022Article
- DNA Polymerase η Promotes the Transcriptional Bypass ofJournal of the American Chemical Society · 2021Article
- Transcriptional processing of an unnatural base pair by eukaryotic RNA polymerase II.Nature chemical biology · 2021Article
- Genome-wide surveillance of transcription errors in response to genotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Molecular basis of transcriptional pausing, stalling, and transcription-coupled repair initiation.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Formation and Recognition of UV-Induced DNA Damage within Genome Complexity.International journal of molecular sciences · 2020Review
- Role of the trigger loop in translesion RNA synthesis by bacterial RNA polymerase.The Journal of biological chemistry · 2020Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
UV-induced cyclobutane pyrimidine dimers (CPDs) in the template DNA strand stall transcription elongation by RNA polymerase II (Pol II). If the nucleotide excision repair machinery does not promptly remove the CPDs, stalled Pol II creates a roadblock for DNA replication and subsequent rounds of transcription. Here we present evidence that Pol II has an intrinsic capacity for translesion synthesis (TLS) that enables bypass of the CPD with or without repair. Translesion synthesis depends on the trigger loop and bridge helix, the two flexible regions of the Pol II subunit Rpb1 that participate in substrate binding, catalysis, and translocation. Substitutions in Rpb1 that promote lesion bypass in vitro increase UV resistance in vivo, and substitutions that inhibit lesion bypass decrease cell survival after UV irradiation. Thus, translesion transcription becomes essential for cell survival upon accumulation of the unrepaired CPD lesions in genomic DNA.
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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.