ArticleJournal of bacteriology2003
Quinolone resistance due to reduced target enzyme expression.
Article in Journal of bacteriology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 72 citations in OpenAlex.
- Marine Bacteria as a Source of Antibiotics AgainstMarine drugs · 2026Review
- Antibacterial Mechanisms and Clinical Impact of Sitafloxacin.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Gyrase and Topoisomerase IV: Recycling Old Targets for New Antibacterials to Combat Fluoroquinolone Resistance.ACS infectious diseases · 2024Review
- Antimicrobial resistance and associated risk factors inVeterinary world · 2024Article
- Unusual and Unconsidered Mechanisms of Bacterial Resilience and Resistance to Quinolones.Life (Basel, Switzerland) · 2024Review
- Optimal effective concentration combinations (OPECCs) for binary application of membrane-targeting antiseptics and TMPyP-mediated antimicrobial photodynamic therapy.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024Article
- Collateral sensitivity profiling in drug-resistant Escherichia coli identifies natural products suppressing cephalosporin resistance.Nature communications · 2023Article
- Molecular co-localization of multiple drugs in a nanoscopic delivery vehicle for potential synergistic remediation of multi-drug resistant bacteria.Scientific reports · 2022Article
- The evolving biology ofFrontiers in cellular and infection microbiology · 2022Review
- Quinolones: Mechanism, Lethality and Their Contributions to Antibiotic Resistance.Molecules (Basel, Switzerland) · 2020Review
- Transferable Mechanisms of Quinolone Resistance from 1998 Onward.Clinical microbiology reviews · 2019Review
- A role for topoisomerase III in Escherichia coli chromosome segregation.Molecular microbiology · 2012Article
- Emerging fluoroquinolone resistance in Streptococcus agalactiae in South Korea.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2012Article
- Mechanism of action of the arylomycin antibiotics and effects of signal peptidase I inhibition.Antimicrobial agents and chemotherapy · 2012Article
- A fluoroquinolone resistance associated mutation in gyrA Affects DNA supercoiling in Campylobacter jejuni.Frontiers in cellular and infection microbiology · 2012Article
- Global fluoroquinolone resistance epidemiology and implictions for clinical use.Interdisciplinary perspectives on infectious diseases · 2012Article
- High-frequency transposition for determining antibacterial mode of action.Nature chemical biology · 2011Article
- Challenges of antibacterial discovery.Clinical microbiology reviews · 2011Review
- Staphylococcus aureus TargetArray: comprehensive differential essential gene expression as a mechanistic tool to profile antibacterials.Antimicrobial agents and chemotherapy · 2010Article
- Antibiotic resistance and its cost: is it possible to reverse resistance?Nature reviews. Microbiology · 2010Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We report for the first time low-level quinolone resistance mediated by decreased expression of topoisomerase IV in Staphylococcus aureus. A single-step mutant of wild-type S. aureus strain ISP794, P18 selected by using twice the MIC of premafloxacin, had four- and four- to eightfold greater MICs of premafloxacin and ciprofloxacin, respectively, than the wild type. Sequencing of parEC and gyrBA with their promoter regions revealed a point mutation (G-->A) 13 bp upstream of the start codon of parE. Genetic linkage studies showed that there was a high level of correlation between the mutation and the resistance phenotype, and allelic exchange confirmed the contribution of the mutation to resistance. Decreased expression of ParE and decreased steady-state levels of parEC transcripts in P18 and in resistant allelic exchange mutants were observed. The steady-state levels of gyrBA and topB transcripts were increased in P18 but not in two resistant allelic exchange mutants, and sequencing upstream of either gene did not reveal a difference between ISP794 and P18. The steady-state levels of topA transcripts were similar in the various strains. Growth competition experiments performed at 30, 37, and 41 degrees C with a susceptible allelic exchange strain and a resistant allelic exchange strain suggested that loss of fitness was associated with reduced levels of ParE at 41 degrees C. However, P18 had a growth advantage over ISP794 at all temperatures, suggesting that a compensatory mechanism was associated with the increased levels of gyrBA and topB transcripts. Thus, reduced levels of ParE appear to be compatible with cell survival, although there may be a fitness cost during rapid cell multiplication, which might be overcome by compensatory mechanisms without reversion of the resistance phenotype.
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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.