ArticleThe Journal of biological chemistry2019
Error-prone replication of a 5-formylcytosine-mediated DNA-peptide cross-link in human cells.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Protein-Protein Cross-Linking by a DNA Damage-Derived Histone Modification.Journal of the American Chemical Society · 2026Article
- Peptide Sequence and Cross-Link Structure Influence Translesion Synthesis Polymerase Bypass of 5-Formylcytosine-Mediated DNA-Peptide Cross-Links.Chemical research in toxicology · 2025Article
- Mechanisms underlying low mutation rates in mammalian oocytes and preimplantation embryos.Nucleic acids research · 2025Review
- Endogenous Cellular Metabolite Methylglyoxal Induces DNA-Protein Cross-Links in Living Cells.ACS chemical biology · 2024Article
- Incorporation of inosine into DNA by human polymerase eta (Polη): kinetics of nucleotide misincorporation and structural basis for the mutagenicity.The Biochemical journal · 2023Article
- Abasic site-peptide cross-links are blocking lesions repaired by AP endonucleases.Nucleic acids research · 2023Article
- Bypass of Abasic Site-Peptide Cross-Links by Human Repair and Translesion DNA Polymerases.International journal of molecular sciences · 2023Article
- Establishing Linkages Among DNA Damage, Mutagenesis, and Genetic Diseases.Chemical research in toxicology · 2022Review
- Sequence context effects of replication of Fapy•dG in three mutational hot spot sequences of the p53 gene in human cells.DNA repair · 2021Article
- DNA polymerases η and κ bypass NThe Journal of biological chemistry · 2021Article
- Comparative Nucleosomal Reactivity of 5-Formyl-Uridine and 5-Formyl-Cytidine.Chemistry (Weinheim an der Bergstrasse, Germany) · 2021Article
- Translesion Synthesis Past 5-Formylcytosine-Mediated DNA-Peptide Cross-Links by hPolη Is Dependent on the Local DNA Sequence.Biochemistry · 2021Article
- DNA polymerase ι compensates for Fanconi anemia pathway deficiency by countering DNA replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Mutagenic Effects of a 2-Deoxyribonolactone-Thymine Glycol Tandem DNA Lesion in Human Cells.Biochemistry · 2020Article
- Transcriptional Bypass of DNA-Protein and DNA-Peptide Conjugates by T7 RNA Polymerase.ACS chemical biology · 2019Article
- Enzymatic bypass of an NThe Journal of biological chemistryArticle
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
DNA-protein cross-links can interfere with chromatin architecture, block DNA replication and transcription, and interfere with DNA repair. Here we synthesized a DNA 23-mer containing a site-specific DNA-peptide cross-link (DpC) by cross-linking an 11-mer peptide to the DNA epigenetic mark 5-formylcytosine in synthetic DNA and used it to generate a DpC-containing plasmid construct. Upon replication of the DpC-containing plasmid in HEK 293T cells, approximately 9% of progeny plasmids contained targeted mutations and 5% semitargeted mutations. Targeted mutations included C→T transitions and C deletions, whereas semitargeted mutations included several base substitutions and deletions near the DpC lesion. To identify DNA polymerases involved in DpC bypass, we comparatively studied translesion synthesis (TLS) efficiency and mutagenesis of the DpC in a series of cell lines with TLS polymerase knockouts or knockdowns. Knockdown of either hPol ι or hPol ζ reduced the mutation frequency by nearly 50%. However, the most significant reduction in mutation frequency (50%-70%) was observed upon simultaneous knockout of hPol η and hPol κ with knockdown of hPol ζ, suggesting that these TLS polymerases play a critical role in error-prone DpC bypass. Because TLS efficiency of the DpC construct was not significantly affected in TLS polymerase-deficient cells, we examined a possible role of replicative DNA polymerases in their bypass and determined that hPol δ and hPol ϵ can accurately bypass the DpC. We conclude that both replicative and TLS polymerases can bypass this DpC lesion in human cells but that mutations are induced mainly by TLS polymerases.
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