ArticleGenome biology2018
Genomic landscape of oxidative DNA damage and repair reveals regioselective protection from mutagenesis.
Article in Genome biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 135 citations in OpenAlex.
- Aspects of plant intelligence (ii).Plant signaling & behavior · 2026Review
- Using the DNA language model, GROVER, to parse effects of sequence, chromatin and regulatory features on genome stability.Bioinformatics (Oxford, England) · 2026Article
- DNA Structure-Dependent Enrichment of Oxidative Lesions.Chemical research in toxicology · 2026Article
- 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
- Mapping DNA glycosylase binding across lesion sequence contexts reveals extended sequence and structural recognition logic.Nature communications · 2026Article
- Genes shielded, repeats exposed: mutation bias in the midge Chironomus riparius.G3 (Bethesda, Md.) · 2026Article
- DamageFormer: a damage-aware multimodal deep learning framework for DNA lesion identification from nanopore sequencing.bioRxiv : the preprint server for biology · 2026Article
- Linking somatic mutations in cancer to the electronic properties of DNA.BMC genomics · 2026Article
- Click-code-seq reveals strand biases of DNA oxidation and depurination in human genome.Nature chemical biology · 2026Article
- Melanin as a Redox Hub: Linking Energy Flow to Genome Stability and Immune Control.Antioxidants & redox signaling · 2026Review
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- Evaluation of ensilication technology for ambient DNA preservation.NAR molecular medicine · 2026Article
- The impact of high-sugar diets on central nervous system disorders: mechanisms, pathogenesis, and dietary implication.Annals of medicine · 2025Review
- The 'vulnerability code': Is cell identity the architect of its own decay?Clinical and translational medicine · 2025Article
- Dynamic genome-wide mapping reveals how chromatin context shapes OGG1-mediated repair and related mutagenesis in human cells.Nucleic acids research · 2025Article
- ADP-ribosylation of NuMA promotes DNA single-strand break repair and transcription.Cell reports · 2025Article
- Direct detection of 8-oxo-dG using nanopore sequencing.Nature communications · 2025Article
- Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability.Nature methods · 2025Article
- Review
- Methods and applications of genome-wide profiling of DNA damage and rare mutations.Nature reviews. Genetics · 2024Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundDNA is subject to constant chemical modification and damage, which eventually results in variable mutation rates throughout the genome. Although detailed molecular mechanisms of DNA damage and repair are well understood, damage impact and execution of repair across a genome remain poorly defined.
resultsTo bridge the gap between our understanding of DNA repair and mutation distributions, we developed a novel method, AP-seq, capable of mapping apurinic sites and 8-oxo-7,8-dihydroguanine bases at approximately 250-bp resolution on a genome-wide scale. We directly demonstrate that the accumulation rate of apurinic sites varies widely across the genome, with hot spots acquiring many times more damage than cold spots. Unlike single nucleotide variants (SNVs) in cancers, damage burden correlates with marks for open chromatin notably H3K9ac and H3K4me2. Apurinic sites and oxidative damage are also highly enriched in transposable elements and other repetitive sequences. In contrast, we observe a reduction at chromatin loop anchors with increased damage load towards inactive compartments. Less damage is found at promoters, exons, and termination sites, but not introns, in a seemingly transcription-independent but GC content-dependent manner. Leveraging cancer genomic data, we also find locally reduced SNV rates in promoters, coding sequence, and other functional elements.
conclusionsOur study reveals that oxidative DNA damage accumulation and repair differ strongly across the genome, but culminate in a previously unappreciated mechanism that safeguards the regulatory and coding regions of genes from mutations.
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Registered trials
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.