ArticleProceedings of the National Academy of Sciences of the United States of America2018
Structural basis of transcriptional stalling and bypass of abasic DNA lesion by RNA polymerase II.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Molecular basis of nick ligation in the nucleosome by DNA Ligase IIIα.Nature communications · 2026Article
- Topology Resetting During Transcription-Coupled Nucleotide Excision Repair.International journal of molecular sciences · 2026Review
- DEPACE-seq enables high-fidelity, single-nucleotide-resolution mapping of abasic sites and characterization of dynamic and long-lived AP landscapes in mammalian genomes.Nucleic acids research · 2026Article
- Structural basis of nucleosome remodeling by Cockayne syndrome B homologue Komagataella phaffii Rad26.Nature communications · 2026Article
- When R-Loops Go Awry: Genome Instability and Neurological Diseases.The European journal of neuroscience · 2026Review
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Widespread epistasis shapes RNA polymerase II active site function and evolution.Nature communications · 2025Article
- The function of MYC in base excision repair protects against RAS-induced senescence.Nucleic acids research · 2025Article
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Cryo-EM uncovers a sequential mechanism for RNA polymerase I pausing and stalling at abasic DNA lesions.Nature communications · 2025Article
- RNA Polymerase II Activity Control of Gene Expression and Involvement in Disease.Journal of molecular biology · 2025Review
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Molecular Mechanism of RNA Polymerase II Transcriptional Mutagenesis by the Epimerizable DNA Lesion, Fapy·dG.Journal of the American Chemical Society · 2024Article
- Molecular insight into how the position of an abasic site modifies DNA duplex stability and dynamics.Biophysical journal · 2024Article
- Back-Up Base Excision DNA Repair in Human Cells Deficient in the Major AP Endonuclease, APE1.International journal of molecular sciences · 2023Article
- Genome-wide maps of UVA and UVB mutagenesis in yeast reveal distinct causative lesions and mutational strand asymmetries.Genetics · 2023Article
- Human TDP1, APE1 and TREX1 repair 3'-DNA-peptide/protein cross-links arising from abasic sites in vitro.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
- 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
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5 authors.
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Abstract
Abasic sites are among the most abundant DNA lesions and interfere with DNA replication and transcription, but the mechanism of their action on transcription remains unknown. Here we applied a combined structural and biochemical approach for a comprehensive investigation of how RNA polymerase II (Pol II) processes an abasic site, leading to slow bypass of lesion. Encounter of Pol II with an abasic site involves two consecutive slow steps: insertion of adenine opposite a noninstructive abasic site (the A-rule), followed by extension of the 3'-rAMP with the next cognate nucleotide. Further studies provided structural insights into the A-rule: ATP is slowly incorporated into RNA in the absence of template guidance. Our structure revealed that ATP is bound to the Pol II active site, whereas the abasic site is located at an intermediate state above the Bridge Helix, a conserved structural motif that is cirtical for Pol II activity. The next extension step occurs in a template-dependent manner where a cognate substrate is incorporated, despite at a much slower rate compared with nondamaged template. During the extension step, neither the cognate substrate nor the template base is located at the canonical position, providing a structural explanation as to why this step is as slow as the insertion step. Taken together, our studies provide a comprehensive understanding of Pol II stalling and bypass of the abasic site in the DNA template.
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