ArticleNature genetics2019
Error-prone bypass of DNA lesions during lagging-strand replication is a common source of germline and cancer mutations.
Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- What sets the mutation rate of a cell type in an animal species?PLoS biology · 2026Article
- What sets the mutation rate of a cell type in an animal species?bioRxiv : the preprint server for biology · 2025Article
- Transcription start sites experience a high influx of heritable variants fueled by early development.Nature communications · 2025Article
- Sex differences in transcription-associated mutagenesis in the human germline.bioRxiv : the preprint server for biology · 2025Article
- Article
- Deciphering the Foundations of Mitochondrial Mutational Spectra: Replication-Driven and Damage-Induced Signatures Across Chordate Classes.Molecular biology and evolution · 2025Article
- A tale of two strands: Decoding chromatin replication through strand-specific sequencing.Molecular cell · 2025Review
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Contributing factors to the oxidation-induced mutational landscape in human cells.Nature communications · 2024Article
- Mutational signature analyses in multi-child families reveal sources of age-related increases in human germline mutations.Communications biology · 2024Article
- Article
- The clock-like accumulation of germline and somatic mutations can arise from the interplay of DNA damage and repair.PLoS biology · 2024Article
- Article
- 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
- A mutation rate model at the basepair resolution identifies the mutagenic effect of polymerase III transcription.Nature genetics · 2023Article
- Disentangling sources of clock-like mutations in germline and soma.bioRxiv : the preprint server for biology · 2023Article
- Contributions of replicative and translesion DNA polymerases to mutagenic bypass of canonical and atypical UV photoproducts.Nature communications · 2023Article
- Strand asymmetries across genomic processes.Computational and structural biotechnology journal · 2023Review
- A mitochondria-specific mutational signature of aging: increased rate of A > G substitutions on the heavy strand.Nucleic acids research · 2022Article
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Authors and funding
8 authors at 5 institutions in 5 countries.
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Abstract
Studies in experimental systems have identified a multitude of mutational mechanisms including DNA replication infidelity and DNA damage followed by inefficient repair or replicative bypass. However, the relative contributions of these mechanisms to human germline mutation remain unknown. Here, we show that error-prone damage bypass on the lagging strand plays a major role in human mutagenesis. Transcription-coupled DNA repair removes lesions on the transcribed strand; lesions on the non-transcribed strand are preferentially converted into mutations. In human polymorphism we detect a striking similarity between mutation types predominant on the non-transcribed strand and on the strand lagging during replication. Moreover, damage-induced mutations in cancers accumulate asymmetrically with respect to the direction of replication, suggesting that DNA lesions are resolved asymmetrically. We experimentally demonstrate that replication delay greatly attenuates the mutagenic effect of ultraviolet irradiation, confirming that replication converts DNA damage into mutations. We estimate that at least 10% of human mutations arise due to DNA damage.
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