ArticleNucleic acids research2013
Oxidative stress-induced mutagenesis in single-strand DNA occurs primarily at cytosines and is DNA polymerase zeta-dependent only for adenines and guanines.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed, 66 citations in OpenAlex.
- Detection of "hidden" mitotic crossovers by long-read DNA sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Break-induced replication forms long mutable single-strand DNA during meiosis.Nature communications · 2026Article
- Increased replication-associated single-stranded DNA promotes formaldehyde-induced mutagenesis.bioRxiv : the preprint server for biology · 2026Article
- Translesion polymerases and DNA-protein crosslink repair shapes the cellular response to formaldehyde-induced DNA damage in ssDNA.Nucleic acids research · 2025Article
- Loss of Heterozygosity associated with ubiquitous environments in yeast.PLoS genetics · 2025Article
- NOX4 Suppresses Ferroptosis Through Regulation of the Pentose Phosphate Pathway in Colorectal Cancer.Current medical science · 2025Article
- Copper induced augmentation of antibiotic resistance in Acinetobacter baumannii MCC 3114.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Molecular and Clinicopathologic Impact of GNAS Variants Across Solid Tumors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Article
- Effects of the glyphosate-based herbicide roundup on C. elegans and S. cerevisiae mortality, reproduction, and transcription fidelity.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Glycidamide-induced hypermutation in yeast single-stranded DNA reveals a ubiquitous clock-like mutational motif in humans.Nucleic acids research · 2023Article
- Nonlethal Furfural Exposure Causes Genomic Alterations and Adaptability Evolution in Saccharomyces cerevisiae.Microbiology spectrum · 2023Article
- Gut microbes involvement in gastrointestinal cancers through redox regulation.Gut pathogens · 2023Review
- Genome-wide maps of UVA and UVB mutagenesis in yeast reveal distinct causative lesions and mutational strand asymmetries.Genetics · 2023Article
- Oxidative stress drives mutagenesis through transcription-coupled repair in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Changes in metabolic landscapes shape divergent but distinct mutational signatures and cytotoxic consequences of redox stress.Nucleic acids research · 2023Article
- Widely spaced and divergent inverted repeats become a potent source of chromosomal rearrangements in long single-stranded DNA regions.Nucleic acids research · 2023Article
- DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023Review
- Molecular and immunological mechanisms of clonal evolution in multiple myeloma.Frontiers in immunology · 2023Review
- Virus-Like Cytosolic and Cell-Free Oxidatively Damaged Nucleic Acids Likely Drive Inflammation, Synapse Degeneration, and Neuron Death in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Review
- Analyses of mutational patterns induced by formaldehyde and acetaldehyde reveal similarity to a common mutational signature.G3 (Bethesda, Md.) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Localized hyper-mutability caused by accumulation of lesions in persistent single-stranded (ss) DNA has been recently found in several types of cancers. An increase in endogenous levels of reactive oxygen species (ROS) is considered to be one of the hallmarks of cancers. Employing a yeast model system, we addressed the role of oxidative stress as a potential source of hyper-mutability in ssDNA by modulation of the endogenous ROS levels and by exposing cells to oxidative DNA-damaging agents. We report here that under oxidative stress conditions the majority of base substitution mutations in ssDNA are caused by erroneous, DNA polymerase (Pol) zeta-independent bypass of cytosines, resulting in C to T transitions. For all other DNA bases Pol zeta is essential for ROS-induced mutagenesis. The density of ROS-induced mutations in ssDNA is lower, compared to that caused by UV and MMS, which suggests that ssDNA could be actively protected from oxidative damage. These findings have important implications for understanding mechanisms of oxidative mutagenesis, and could be applied to development of anticancer therapies and cancer prevention.
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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.