DNA gyrase Overview
DNA gyrase is an ATP-dependent type II DNA topoisomerase unique to bacteria, composed of two GyrA and two GyrB subunits, forming an A2B2 tetrameric complex. It introduces negative supercoils into closed circular double-stranded DNA, an activity crucial for bacterial DNA replication, transcription, and chromosome segregation. Several classes of antibiotics, most notably fluoroquinolones and aminocoumarins, target DNA gyrase, causing bacterial cell death by disrupting essential DNA topology. Drug resistance, especially via mutated gyrA/gyrB genes, poses a therapeutic challenge, reinforcing DNA gyrase as a central target for antibiotic discovery and development.
Mechanism of Action
Inhibition of DNA gyrase prevents negative supercoiling, blocks DNA replication and transcription, and induces DNA breakage, leading to bacterial death. Fluoroquinolones stabilize DNA gyrase-DNA cleavage complexes, causing double-strand breaks. Aminocoumarins inhibit ATPase activity of the GyrB subunit. Diverse inhibitors may block DNA binding or enzyme catalysis.
Biological Functions
Disease Associations
Safety Considerations
- Selectivity: Drugs must distinguish bacterial DNA gyrase from eukaryotic topoisomerases to avoid off-target effects
- Resistance: Mutations in gyrA/gyrB lead to drug resistance
- Some side effects for fluoroquinolones (tendinopathies, CNS effects)
Interacting Drugs
Associated Biomarkers
Biomarker |
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No standard, clinically-validated biomarkers; resistance genes (gyrA/gyrB mutations) are used in research and diagnostics to monitor drug susceptibility |