ArticleNucleic acids research2025
Dynamic genome-wide mapping reveals how chromatin context shapes OGG1-mediated repair and related mutagenesis in human cells.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The conformation of the complementary strand and the deformation of the DNA groove upon DDB2 binding justifies the different repair rates for cyclobutane pyrimidine dimers.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Contribution of One-Electron Oxidation of Purine and Pyrimidine Bases to the Photo- and Radiation-Induced Damage to Cellular DNA.Chemphyschem : a European journal of chemical physics and physical chemistry · 2026Review
- 8oxoG:A Is Structurally Accommodated in the Nucleosome Core Particle, Yet Inaccessible to MUTYH-Initiated DNA Repair.Biomolecules · 2026Article
- Nucleotide salvage, genome instability, and potential therapeutic applications.Nucleic acids research · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Potassium bromate-induced DNA damage, including 8-oxo-7,8-dihydroguanine (OG) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyG), are common oxidatively generated DNA lesions with mutagenic potential if not efficiently repaired. While sequencing-based studies have shown that damage formation is influenced by DNA sequence context, secondary structures, and chromatin features, how OGG1-mediated repair is regulated within chromatin remains unclear. Here, we apply CLAPS-seq to generate genome-wide, single-nucleotide resolution maps of OGG1-mediated repair over time in human cells, and systematically analyze how chromatin context affects repair efficiency across hierarchical scales. We find that chromatin accessibility governs rapid initial repair, whereas higher-order chromatin structures increasingly influence later-phase repair. In addition, nucleosome occupancy and transcription factor binding, exemplified by CCCTC-binding factor (CTCF), modulate OGG1-mediated repair at both local and base scales. Overall, mutational outcomes correlate more strongly with repair dynamics than with damage levels. Together, these findings establish a comprehensive framework linking chromatin organization, DNA repair kinetics, and oxidatively induced mutagenesis, and offer new insights into the origins of mutation patterns in cancer and diseases associated with oxidative stress.
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