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Updated: Aug 11, 2026

Testing the Role of Multicopy Plasmids in the Evolution of Antibiotic Resistance
Published on: May 2, 2018
In vitro plasmid-encoded resistance to quinolones
J M Gómez-Gómez1, J Blázquez, L E Espinosa De Los Monteros
1Servicio de Microbiología, Hospital Ramón y Cajal, Madrid, Spain.
Plasmid-encoded quinolone resistance can emerge through genetic alterations. A mutant gyrA allele on a plasmid conferred quinolone resistance in susceptible Escherichia coli, demonstrating a mechanism for antibiotic resistance spread.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Antibiotic resistance is a growing global health concern.
- Quinolones are a critical class of antibiotics used to treat bacterial infections.
- Understanding the genetic basis of quinolone resistance is essential for developing effective treatment strategies.
Purpose of the Study:
- To investigate the potential for plasmid-mediated quinolone resistance.
- To explore the role of the gyrA gene in quinolone resistance.
- To demonstrate a mechanism for the spread of quinolone resistance.
Main Methods:
- Two distinct model systems were employed to study quinolone resistance.
- The impact of wild-type gyrA allele dosage on minimum inhibitory concentrations (MICs) was assessed.
- A mutant gyrA allele was cloned into a multicopy plasmid and expressed in a susceptible Escherichia coli strain.
Main Results:
- Increased levels of the wild-type gyrA allele resulted in a moderate increase in quinolone MICs.
- Expression of the mutant gyrA allele from a multicopy plasmid successfully conferred a quinolone resistance phenotype.
- This indicates that plasmid-borne gyrA mutations can drive resistance.
Conclusions:
- Plasmids can indeed carry and express genes conferring quinolone resistance.
- The gyrA gene is a key target for quinolone action and mutations within it can lead to resistance.
- Plasmid-mediated resistance presents a significant challenge for antibiotic therapy and necessitates further research into resistance mechanisms and control.
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