ArticleNucleic acids research2016
Mechanism of fusidic acid inhibition of RRF- and EF-G-dependent splitting of the bacterial post-termination ribosome.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Structural characterization of ribosome recycling and fusidic acid inhibition in Staphylococcus aureus.Nucleic acids research · 2026Article
- Proteotoxic Stress Bioreporter Enables Mechanism-Informed Antibiotic Discovery.Journal of natural products · 2026Article
- Mechanisms of fusidic acid resistance.Biochemical Society transactions · 2025Review
- Structures of the Staphylococcus aureus ribosome inhibited by fusidic acid and fusidic acid cyclopentane.Scientific reports · 2024Article
- Enhancing the Topical Antibacterial Activity of Fusidic Acid via Embedding into Cinnamon Oil Nano-Lipid Carrier.Gels (Basel, Switzerland) · 2024Article
- Reversing the Natural Drug Resistance of Gram-Negative Bacteria to Fusidic Acid via Forming Drug-Phospholipid Complex.Bioengineering (Basel, Switzerland) · 2024Article
- Ribosome Protection Proteins-"New" Players in the Global Arms Race with Antibiotic-Resistant Pathogens.International journal of molecular sciences · 2021Review
- High-Resolution DNA Dual-Rulers Reveal a New Intermediate State in Ribosomal Frameshifting.Chembiochem : a European journal of chemical biology · 2021Article
- A Quick Guide to Small-Molecule Inhibitors of Eukaryotic Protein Synthesis.Biochemistry. Biokhimiia · 2020Review
- Analysis of multidrug resistance inVirulence · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The antibiotic drug fusidic acid (FA) is commonly used in the clinic against gram-positive bacterial infections. FA targets ribosome-bound elongation factor G (EF-G), a translational GTPase that accelerates both messenger RNA (mRNA) translocation and ribosome recycling. How FA inhibits translocation was recently clarified, but FA inhibition of ribosome recycling by EF-G and ribosome recycling factor (RRF) has remained obscure. Here we use fast kinetics techniques to estimate mean times of ribosome splitting and the stoichiometry of GTP hydrolysis by EF-G at varying concentrations of FA, EF-G and RRF. These mean times together with previous data on uninhibited ribosome recycling were used to clarify the mechanism of FA inhibition of ribosome splitting. The biochemical data on FA inhibition of translocation and recycling were used to model the growth inhibitory effect of FA on bacterial populations. We conclude that FA inhibition of translocation provides the dominant cause of bacterial growth reduction, but that FA inhibition of ribosome recycling may contribute significantly to FA-induced expression of short regulatory open reading frames, like those involved in FA resistance.
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