ArticleProceedings of the National Academy of Sciences of the United States of America2015
Mechanism of RNA polymerase II bypass of oxidative cyclopurine DNA lesions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Transcriptional stress in aging: integrating experimental data and modeling to quantify DNA damage accumulation.Frontiers in molecular biosciences · 2025Article
- Replication-Independent ICL Repair: From Chemotherapy to Cell Homeostasis.Journal of molecular biology · 2024Review
- Molecular Mechanism of RNA Polymerase II Transcriptional Mutagenesis by the Epimerizable DNA Lesion, Fapy·dG.Journal of the American Chemical Society · 2024Article
- 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
- RNA polymerase II trapped on a molecular treadmill: Structural basis of persistent transcriptional arrest by a minor groove DNA binder.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Incorporation of 5',8-cyclo-2'deoxyadenosines by DNA repair polymerases via base excision repair.DNA repair · 2022Article
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- 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
- The Influence of 5'Molecules (Basel, Switzerland) · 2021Article
- Molecular basis of transcriptional pausing, stalling, and transcription-coupled repair initiation.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Role of the trigger loop in translesion RNA synthesis by bacterial RNA polymerase.The Journal of biological chemistry · 2020Article
- RNA polymerase II stalls on oxidative DNA damage via a torsion-latch mechanism involving lone pair-π and CH-π interactions.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
- The Influence of (5'Cells · 2019Article
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9 authors.
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Abstract
In human cells, the oxidative DNA lesion 8,5'-cyclo-2'-deoxyadenosine (CydA) induces prolonged stalling of RNA polymerase II (Pol II) followed by transcriptional bypass, generating both error-free and mutant transcripts with AMP misincorporated immediately downstream from the lesion. Here, we present biochemical and crystallographic evidence for the mechanism of CydA recognition. Pol II stalling results from impaired loading of the template base (5') next to CydA into the active site, leading to preferential AMP misincorporation. Such predominant AMP insertion, which also occurs at an abasic site, is unaffected by the identity of the 5'-templating base, indicating that it derives from nontemplated synthesis according to an A rule known for DNA polymerases and recently identified for Pol II bypass of pyrimidine dimers. Subsequent to AMP misincorporation, Pol II encounters a major translocation block that is slowly overcome. Thus, the translocation block combined with the poor extension of the dA.rA mispair reduce transcriptional mutagenesis. Moreover, increasing the active-site flexibility by mutation in the trigger loop, which increases the ability of Pol II to accommodate the bulky lesion, and addition of transacting factor TFIIF facilitate CydA bypass. Thus, blocking lesion entry to the active site, translesion A rule synthesis, and translocation block are common features of transcription across different bulky DNA lesions.
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