ArticleProceedings of the National Academy of Sciences of the United States of America2013
Genomic assay reveals tolerance of DNA damage by both translesion DNA synthesis and homology-dependent repair in mammalian cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- TET2 loss triggers ssDNA gap accumulation and heightened PARP inhibitor sensitivity.Nature communications · 2026Article
- PCNA encircling primer/template junctions is eliminated by exchange of RPA for Rad51: implications for the interplay between human DNA damage tolerance pathways.Nucleic acids research · 2026Article
- Article
- Replication gap suppression depends on the double-strand DNA binding activity of BRCA2.Nature communications · 2023Article
- Establishing Linkages Among DNA Damage, Mutagenesis, and Genetic Diseases.Chemical research in toxicology · 2022Review
- Translesion synthesis of apurinic/apyrimidic site analogues by Y-family DNA polymerase Dbh fromActa biochimica et biophysica Sinica · 2022Article
- To skip or not to skip: choosing repriming to tolerate DNA damage.Molecular cell · 2021Review
- PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts.Nature communications · 2020Article
- EGFP Reporters for Direct and Sensitive Detection of Mutagenic Bypass of DNA Lesions.Biomolecules · 2020Article
- Regulation of HLTF-mediated PCNA polyubiquitination by RFC and PCNA monoubiquitination levels determines choice of damage tolerance pathway.Nucleic acids research · 2018Article
- Chronological Switch from Translesion Synthesis to Homology-Dependent Gap RepairToxicological research · 2018Review
- BPDE-induced genotoxicity: relationship between DNA adducts, mutagenicity in the in vitro PIG-A assay, and the transcriptional response to DNA damage in TK6 cells.Archives of toxicology · 2018Article
- DNA-dependent protease activity of human Spartan facilitates replication of DNA-protein crosslink-containing DNA.Nucleic acids research · 2017Article
- Mechanisms of Post-Replication DNA Repair.Genes · 2017Review
- Mass Spectrometry-Based Quantitative Strategies for Assessing the Biological Consequences and Repair of DNA Adducts.Accounts of chemical research · 2016Review
- Nucleotide Excision Repair and Transcription-coupled DNA Repair Abrogate the Impact of DNA Damage on Transcription.The Journal of biological chemistry · 2016Article
- Human HLTF mediates postreplication repair by its HIRAN domain-dependent replication fork remodelling.Nucleic acids research · 2015Article
- DNA sequence context greatly affects the accuracy of bypass across an ultraviolet light 6-4 photoproduct in mammalian cells.Mutation research · 2015Article
- Article
- The identification of translesion DNA synthesis regulators: Inhibitors in the spotlight.DNA repair · 2015Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
DNA lesions can block replication forks and lead to the formation of single-stranded gaps. These replication complications are mitigated by DNA damage tolerance mechanisms, which prevent deleterious outcomes such as cell death, genomic instability, and carcinogenesis. The two main tolerance strategies are translesion DNA synthesis (TLS), in which low-fidelity DNA polymerases bypass the blocking lesion, and homology-dependent repair (HDR; postreplication repair), which is based on the homologous sister chromatid. Here we describe a unique high-resolution method for the simultaneous analysis of TLS and HDR across defined DNA lesions in mammalian genomes. The method is based on insertion of plasmids carrying defined site-specific DNA lesions into mammalian chromosomes, using phage integrase-mediated integration. Using this method we show that mammalian cells use HDR to tolerate DNA damage in their genome. Moreover, analysis of the tolerance of the UV light-induced 6-4 photoproduct, the tobacco smoke-induced benzo[a]pyrene-guanine adduct, and an artificial trimethylene insert shows that each of these three lesions is tolerated by both TLS and HDR. We also determined the specificity of nucleotide insertion opposite these lesions during TLS in human genomes. This unique method will be useful in elucidating the mechanism of DNA damage tolerance in mammalian chromosomes and their connection to pathological processes such as carcinogenesis.
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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.