ArticleNature communications2022
BRCA1 deficiency specific base substitution mutagenesis is dependent on translesion synthesis and regulated by 53BP1.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- PARG inhibition reduces ssDNA levels and limits RPA loading upon replication fork collapse.EMBO reports · 2026Article
- USP1 inhibition promotes RAD18-dependent PCNA degradation and BRCA1 synthetic lethality.bioRxiv : the preprint server for biology · 2026Article
- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Nature communications · 2026Article
- Endogenous and environmental factors that induce DNA replication defects and genomic instability in ER-negative heterozygous BRCA1 cells.Scientific reports · 2026Article
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- NNature reviews. Cancer · 2026Review
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Long-term exposure to the ethanol-derived metabolite acetaldehyde elevates structural genomic alterations but not base substitutions.Communications biology · 2026Article
- Tissue-specific mutagenesis from endogenous guanine damage is suppressed by Polκ and DNA repair.Nature communications · 2025Article
- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Research square · 2025Article
- Joint inference of mutational signatures from indels and single-nucleotide substitutions reveals prognostic impact of DNA repair deficiencies.Genome medicine · 2025Article
- Catalytic and noncatalytic functions of DNA polymerase κ in translesion DNA synthesis.Nature structural & molecular biology · 2025Article
- Patterns of spontaneous and induced genomic alterations inApplied and environmental microbiology · 2025Article
- Deaminase-Driven Reverse Transcription Mutagenesis in Oncogenesis: Critical Analysis of Transcriptional Strand Asymmetries of Single Base Substitution Signatures.International journal of molecular sciences · 2025Review
- Whole genome sequencing revealed esophageal squamous cell carcinoma related biomarkers.PloS one · 2025Article
- Article
- RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Recent Advances in Genomic Approaches for the Detection of Homologous Recombination Deficiency.Cancer research and treatment · 2024Review
- Review
- Endogenous base damage as a driver of genomic instability in homologous recombination-deficient cancers.DNA repair · 2024Review
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Authors and funding
13 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defects in BRCA1, BRCA2 and other genes of the homology-dependent DNA repair (HR) pathway cause an elevated rate of mutagenesis, eliciting specific mutation patterns including COSMIC signature SBS3. Using genome sequencing of knock-out cell lines we show that Y family translesion synthesis (TLS) polymerases contribute to the spontaneous generation of base substitution and short insertion/deletion mutations in BRCA1 deficient cells, and that TLS on DNA adducts is increased in BRCA1 and BRCA2 mutants. The inactivation of 53BP1 in BRCA1 mutant cells markedly reduces TLS-specific mutagenesis, and rescues the deficiency of template switch-mediated gene conversions in the immunoglobulin V locus of BRCA1 mutant chicken DT40 cells. 53BP1 also promotes TLS in human cellular extracts in vitro. Our results show that HR deficiency-specific mutagenesis is largely caused by TLS, and suggest a function for 53BP1 in regulating the choice between TLS and error-free template switching in replicative DNA damage bypass.
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