ArticleMolecular microbiology2005
Norfloxacin-induced DNA gyrase cleavage complexes block Escherichia coli replication forks, causing double-stranded breaks in vivo.
Article in Molecular microbiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 76 citations in OpenAlex.
- Genetic analysis of epistasis between nucleotide excision repair and homologous recombination in the recovery of persisters after fluoroquinolone treatment.PLoS genetics · 2026Article
- Dysregulation of a nucleotidyltransferase induces division and surface glycan defects inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Global Challenge of Antimicrobial Resistance: Mechanisms, Case Studies, and Mitigation Approaches.Health science reports · 2025Article
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Gyrase and Topoisomerase IV: Recycling Old Targets for New Antibacterials to Combat Fluoroquinolone Resistance.ACS infectious diseases · 2024Review
- TisB protein is the single molecular determinant underlying multiple downstream effects of ofloxacin inScience advances · 2024Article
- Unusual and Unconsidered Mechanisms of Bacterial Resilience and Resistance to Quinolones.Life (Basel, Switzerland) · 2024Review
- Widespread prevalence of a methylation-dependent switch to activate an essential DNA damage response in bacteria.PLoS biology · 2024Article
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Bacterial Argonaute Proteins Aid Cell Division in the Presence of Topoisomerase Inhibitors in Escherichia coli.Microbiology spectrum · 2023Article
- Antibiotics and Bacterial Resistance-A Short Story of an Endless Arms Race.International journal of molecular sciences · 2023Review
- Mechanistic insight into the repair of C8-linked pyrrolobenzodiazepine monomer-mediated DNA damage.RSC medicinal chemistry · 2022Article
- Role for DNA double strand end-resection activity of RecBCD in control of aberrant chromosomal replication initiation in Escherichia coli.Nucleic acids research · 2022Article
- Growth-dependent heterogeneity in the DNA damage response in Escherichia coli.Molecular systems biology · 2022Article
- Mechanisms and Regulation of DNA-Protein Crosslink Repair During DNA Replication by SPRTN Protease.Frontiers in molecular biosciences · 2022Review
- Ploidy is an important determinant of fluoroquinolone persister survival.Current biology : CB · 2021Article
- Quinolones: Mechanism, Lethality and Their Contributions to Antibiotic Resistance.Molecules (Basel, Switzerland) · 2020Review
- DNA topoisomerase IIIβ promotes cyst generation by inducing cyst wall protein gene expression inOpen biology · 2020Article
- Our Evolving Understanding of the Mechanism of Quinolones.Antibiotics (Basel, Switzerland) · 2018Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Antibacterial quinolones inhibit type II DNA topoisomerases by stabilizing covalent topoisomerase-DNA cleavage complexes, which are apparently transformed into double-stranded breaks by cellular processes such as replication. We used plasmid pBR322 and two-dimensional agarose gel electrophoresis to examine the collision of replication forks with quinolone-induced gyrase-DNA cleavage complexes in Escherichia coli. Restriction endonuclease-digested DNA exhibited a bubble arc with discrete spots, indicating that replication forks had been stalled. The most prominent spot depended upon the strong gyrase binding site of pBR322, providing direct evidence that quinolone-induced cleavage complexes block bacterial replication forks in vivo. We differentiated between stalled forks that do or do not contain bound cleavage complex by extracting DNA under different conditions. Resealing conditions allow gyrase to efficiently reseal the transient breaks within cleavage complexes, while cleavage conditions cause the latent breaks to be revealed. These experiments showed that some stalled forks did not contain a cleavage complex, implying that gyrase had dissociated in vivo and yet the fork had not restarted at the time of DNA isolation. Additionally, some branched plasmid DNA isolated under resealing conditions nonetheless contained broken DNA ends. We discuss a model for the creation of double-stranded breaks by an indirect mechanism after quinolone treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.