ArticleDNA repair2016
Prompt repair of hydrogen peroxide-induced DNA lesions prevents catastrophic chromosomal fragmentation.
Article in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Structural basis for the mechanism and stability of the EEPD1 5' endonuclease.The Journal of biological chemistry · 2026Article
- Acute exposure to high concentrations of polystyrene nanoparticles induces genotoxicity in Daphnia pulex.Environmental science and pollution research international · 2026Article
- Comprehensive Measurement of Inter-Individual Variation in DNA Repair Capacity in Healthy Individuals.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Assessment of Antioxidant Activity and Dose-Dependent Effect on Genotoxicity/Antigenotoxicity ofPharmaceutics · 2025Article
- Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence.Antioxidants (Basel, Switzerland) · 2024Article
- The role of DNA polymerase I in tolerating single-strand breaks generated at clustered DNA damage in Escherichia coli.Scientific reports · 2024Article
- Bacterial nucleoid is a riddle wrapped in a mystery inside an enigma.Journal of bacteriology · 2024Review
- Oxidative stress drives mutagenesis through transcription-coupled repair in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- EEPD1 promotes repair of oxidatively-stressed replication forks.NAR cancer · 2023Article
- Catastrophic chromosome fragmentation probes the nucleoid structure and dynamics in Escherichia coli.Nucleic acids research · 2022Article
- Thymine-starvation-induced chromosomal fragmentation is not required for thymineless death in Escherichia coli.Molecular microbiology · 2022Article
- Nitric oxide precipitates catastrophic chromosome fragmentation by bolstering both hydrogen peroxide and Fe(II) Fenton reactants in E. coli.The Journal of biological chemistry · 2022Article
- Oxidative Damage Blocks Thymineless Death and Trimethoprim Poisoning in Escherichia coli.Journal of bacteriology · 2022Article
- Catalase inhibition by nitric oxide potentiates hydrogen peroxide to trigger catastrophic chromosome fragmentation in Escherichia coli.Genetics · 2021Article
- Article
- Linking high GC content to the repair of double strand breaks in prokaryotic genomes.PLoS genetics · 2019Article
- Visualization and prediction of CRISPR incidence in microbial trait-space to identify drivers of antiviral immune strategy.The ISME journal · 2019Article
- Rescue of DNA damage after constricted migration reveals a mechano-regulated threshold for cell cycle.The Journal of cell biology · 2019Article
- Genome-wide analysis of genomic alterations induced by oxidative DNA damage in yeast.Nucleic acids research · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Iron-dependent oxidative DNA damage in vivo by hydrogen peroxide (H2O2, HP) induces copious single-strand(ss)-breaks and base modifications. HP also causes infrequent double-strand DNA breaks, whose relationship to the cell killing is unclear. Since hydrogen peroxide only fragments chromosomes in growing cells, these double-strand breaks were thought to represent replication forks collapsed at direct or excision ss-breaks and to be fully reparable. We have recently reported that hydrogen peroxide kills Escherichia coli by inducing catastrophic chromosome fragmentation, while cyanide (CN) potentiates both the killing and fragmentation. Remarkably, the extreme density of CN+HP-induced chromosomal double-strand breaks makes involvement of replication forks unlikely. Here we show that this massive fragmentation is further amplified by inactivation of ss-break repair or base-excision repair, suggesting that unrepaired primary DNA lesions are directly converted into double-strand breaks. Indeed, blocking DNA replication lowers CN+HP-induced fragmentation only ∼2-fold, without affecting the survival. Once cyanide is removed, recombinational repair in E. coli can mend several double-strand breaks, but cannot mend ∼100 breaks spread over the entire chromosome. Therefore, double-strand breaks induced by oxidative damage happen at the sites of unrepaired primary one-strand DNA lesions, are independent of replication and are highly lethal, supporting the model of clustered ss-breaks at the sites of stable DNA-iron complexes.
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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.