ArticleNucleic acids research2013
Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.
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 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
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- Deep visual proteomics reveals DNA replication stress as a hallmark of signet ring cell carcinoma.NPJ precision oncology · 2025Article
- The role of DNA polymerase I in tolerating single-strand breaks generated at clustered DNA damage in Escherichia coli.Scientific reports · 2024Article
- 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024Review
- Gut microbes involvement in gastrointestinal cancers through redox regulation.Gut pathogens · 2023Review
- 8-Oxoguanine: from oxidative damage to epigenetic and epitranscriptional modification.Experimental & molecular medicine · 2022Review
- Antioxidant Systems, lncRNAs, and Tunneling Nanotubes in Cell Death Rescue from Cigarette Smoke Exposure.Cells · 2022Review
- AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations.Environmental and molecular mutagenesis · 2022Article
- Therapeutic Opportunities of Disrupting Genome Integrity in Adult Diffuse Glioma.Biomedicines · 2022Review
- Investigating the Anticancer Potential of Salvicine as a Modulator of Topoisomerase II and ROS Signaling Cascade.Frontiers in oncology · 2022Review
- Lysophosphatidic acid suppresses apoptosis of high-grade serous ovarian cancer cells by inducing autophagy activity and promotes cell-cycle progressionFrontiers in pharmacology · 2022Article
- Article
- SOG1 transcription factor promotes the onset of endoreduplication under salinity stress in Arabidopsis.Scientific reports · 2021Article
- The circadian clock ensures successful DNA replication in cyanobacteria.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Influence of Arg399Gln, Arg280His and Arg194Trp XRCC1 gene polymorphisms of Base Excision Repair pathway on the level of 8-oxo-guanine and risk of head and neck cancer in the Polish population.Cancer biomarkers : section A of Disease markers · 2021Article
- Strand with mutagenic lesion is preferentially used as a template in the region of a bi-stranded clustered DNA damage site in Escherichia coli.Scientific reports · 2020Article
- The genomics of oxidative DNA damage, repair, and resulting mutagenesis.Computational and structural biotechnology journal · 2020Review
- Targeting G-quadruplexes with Organic Dyes: Chelerythrine-DNA Binding Elucidated by Combining Molecular Modeling and Optical Spectroscopy.Antioxidants (Basel, Switzerland) · 2019Article
- ROS and the DNA damage response in cancer.Redox biology · 2019Review
- Genomic landscape of oxidative DNA damage and repair reveals regioselective protection from mutagenesis.Genome biology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unresolved repair of clustered DNA lesions can lead to the formation of deleterious double strand breaks (DSB) or to mutation induction. Here, we investigated the outcome of clusters composed of base lesions for which base excision repair enzymes have different kinetics of excision/incision. We designed multiply damaged sites (MDS) composed of a rapidly excised uracil (U) and two oxidized bases, 5-hydroxyuracil (hU) and 8-oxoguanine (oG), excised more slowly. Plasmids harboring these U-oG/hU MDS-carrying duplexes were introduced into Escherichia coli cells either wild type or deficient for DNA n-glycosylases. Induction of DSB was estimated from plasmid survival and mutagenesis determined by sequencing of surviving clones. We show that a large majority of MDS is converted to DSB, whereas almost all surviving clones are mutated at hU. We demonstrate that mutagenesis at hU is correlated with excision of the U placed on the opposite strand. We propose that excision of U by Ung initiates the loss of U-oG-carrying strand, resulting in enhanced mutagenesis at the lesion present on the opposite strand. Our results highlight the importance of the kinetics of excision by base excision repair DNA n-glycosylases in the processing and fate of MDS and provide evidence for the role of strand loss/replication fork collapse during the processing of MDS on their mutational consequences.
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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.