ArticleThe Journal of biological chemistry2012
Basis of miscoding of the DNA adduct N2,3-ethenoguanine by human Y-family DNA polymerases.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- 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
- The Catalytic Activity of Human REV1 on Undamaged and Damaged DNA.International journal of molecular sciences · 2024Article
- Site-Specific Synthesis of Oligonucleotides Containing 6-Oxo-MChemical research in toxicology · 2021Article
- Etheno adducts: from tRNA modifications to DNA adducts and back to miscoding ribonucleotides.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Review
- Review
- Inflammation-induced DNA damage, mutations and cancer.DNA repair · 2019Review
- Tri-Cyclic Nucleobase Analogs and their Ribosides as Substrates of Purine-Nucleoside Phosphorylases. II Guanine and Isoguanine Derivatives.Molecules (Basel, Switzerland) · 2019Article
- OChemical research in toxicology · 2016Article
- Bypass of DNA-Protein Cross-links Conjugated to the 7-Deazaguanine Position of DNA by Translesion Synthesis Polymerases.The Journal of biological chemistry · 2016Article
- Kinetic analysis of bypass of 7,8-dihydro-8-oxo-2'-deoxyguanosine by the catalytic core of yeast DNA polymerase η.Biochimie · 2016Article
- Mutagenic Bypass of an Oxidized Abasic Lesion-Induced DNA Interstrand Cross-Link Analogue by Human Translesion Synthesis DNA Polymerases.Biochemistry · 2015Article
- Intrinsic mutagenic properties of 5-chlorocytosine: A mechanistic connection between chronic inflammation and cancer.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Next-generation sequencing reveals the biological significance of the N(2),3-ethenoguanine lesion in vivo.Nucleic acids research · 2015Article
- Error-prone translesion synthesis past DNA-peptide cross-links conjugated to the major groove of DNA via C5 of thymidine.The Journal of biological chemistry · 2015Article
- Replication past the butadiene diepoxide-derived DNA adduct S-[4-(N(6)-deoxyadenosinyl)-2,3-dihydroxybutyl]glutathione by DNA polymerases.Chemical research in toxicology · 2013Article
- Mechanisms of mutagenesis: DNA replication in the presence of DNA damage.Mutation research. Reviews in mutation researchReview
- Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
N(2),3-Ethenoguanine (N(2),3-εG) is one of the exocyclic DNA adducts produced by endogenous processes (e.g. lipid peroxidation) and exposure to bioactivated vinyl monomers such as vinyl chloride, which is a known human carcinogen. Existing studies exploring the miscoding potential of this lesion are quite indirect because of the lability of the glycosidic bond. We utilized a 2'-fluoro isostere approach to stabilize this lesion and synthesized oligonucleotides containing 2'-fluoro-N(2),3-ε-2'-deoxyarabinoguanosine to investigate the miscoding potential of N(2),3-εG by Y-family human DNA polymerases (pols). In primer extension assays, pol η and pol κ replicated through N(2),3-εG, whereas pol ι and REV1 yielded only 1-base incorporation. Steady-state kinetics revealed that dCTP incorporation is preferred opposite N(2),3-εG with relative efficiencies in the order of pol κ > REV1 > pol η ≈ pol ι, and dTTP misincorporation is the major miscoding event by all four Y-family human DNA pols. Pol ι had the highest dTTP misincorporation frequency (0.71) followed by pol η (0.63). REV1 misincorporated dTTP and dGTP with much lower frequencies. Crystal structures of pol ι with N(2),3-εG paired to dCTP and dTTP revealed Hoogsteen-like base pairing mechanisms. Two hydrogen bonds were observed in the N(2),3-εG:dCTP base pair, whereas only one appears to be present in the case of the N(2),3-εG:dTTP pair. Base pairing mechanisms derived from the crystal structures explain the slightly favored dCTP insertion for pol ι in steady-state kinetic analysis. Taken together, these results provide a basis for the mutagenic potential of N(2),3-εG.
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