ArticleProceedings of the National Academy of Sciences of the United States of America2018
Timing of DNA damage responses impacts persistence to fluoroquinolones.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 101 citations in OpenAlex.
- Heteroresistance tolerance and persistence in antibiotic treatment failure.Folia microbiologica · 2026Review
- Building-block synthesis as a determinant of antibiotic persistence.Nature communications · 2026Article
- Genetic analysis of epistasis between nucleotide excision repair and homologous recombination in the recovery of persisters after fluoroquinolone treatment.PLoS genetics · 2026Article
- Non-canonical double-stranded DNA break repair in Pseudomonas aeruginosa includes LigD-independent non-homologous end joining.Nucleic acids research · 2026Article
- Beyond metabolic dormancy: metabolic rewiring in bacterial persistence.Nature communications · 2026Review
- Genome-wide screen reveals a universal role of ATP in ciprofloxacin tolerance among genetically distinctmLife · 2026Article
- Stationary-phasemSphere · 2026Article
- Molecular Basis of Persister Awakening and Lag-Phase Recovery inInternational journal of molecular sciences · 2026Review
- Conservation and divergence of ciprofloxacin persister survival mechanisms between Pseudomonas aeruginosa and Escherichia coli.PLoS genetics · 2025Article
- TisB enables antibiotic tolerance in Salmonella by preventing prophage induction through ATP depletion.PLoS pathogens · 2025Article
- Unveiling a Novel Mechanism of Enhanced Secretion, Cargo Loading, and Accelerated Dynamics of Bacterial Extracellular Vesicles Following Antibiotic Exposure.Journal of extracellular vesicles · 2025Article
- Post-fluoroquinolone treatment molecular events and nutrient availability modulatebioRxiv : the preprint server for biology · 2025Article
- Article
- Mutations in the Staphylococcus aureus Global Regulator CodY confer tolerance to an interspecies redox-active antimicrobial.PLoS genetics · 2025Article
- Eradication ofACS infectious diseases · 2024Article
- Mutations in thebioRxiv : the preprint server for biology · 2024Article
- Unveiling the critical roles of cellular metabolism suppression in antibiotic tolerance.npj antimicrobials and resistance · 2024Article
- Article
- Exploring the links between SOS response, mutagenesis, and resistance during the recovery period.Antimicrobial agents and chemotherapy · 2024Article
- Metabolic and transcriptional activities underlie stationary-phaseMicrobiology spectrum · 2024Article
2 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial persisters are subpopulations of phenotypic variants in isogenic cultures that can survive lethal doses of antibiotics. Their tolerances are often attributed to reduced activities of antibiotic targets, which limit corruption and damage in persisters compared with bacteria that die from treatment. However, that model does not hold for nongrowing populations treated with ofloxacin, a fluoroquinolone, where antibiotic-induced damage is comparable between cells that live and those that die. To understand how those persisters achieve this feat, we employed a genetic system that uses orthogonal control of MazF and MazE, a toxin and its cognate antitoxin, to generate model persisters that are uniformly tolerant to ofloxacin. Despite this complete tolerance, MazF model persisters required the same DNA repair machinery (RecA, RecB, and SOS induction) to survive ofloxacin treatment as their nongrowing, WT counterparts and exhibited similar indicators of DNA damage from treatment. Further investigation revealed that, following treatment, the timing of DNA repair was critical to MazF persister survival because, when repair was delayed until after growth and DNA synthesis resumed, survival was compromised. In addition, we found that, with nongrowing, WT planktonic and biofilm populations, stalling the resumption of growth and DNA synthesis after the conclusion of fluoroquinolone treatment with a prevalent type of stress at infection sites (nutrient limitation) led to near complete survival. These findings illustrate that the timing of events, such as DNA repair, following fluoroquinolone treatment is important to persister survival and provide further evidence that knowledge of the postantibiotic recovery period is critical to understanding persistence phenotypes.
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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.