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© Research
Publication : PLoS genetics

Oxidative stress antagonizes fluoroquinolone drug sensitivity via the SoxR-SUF Fe-S cluster homeostatic axis.

Team: Stress Adaptation and Metabolism (SAMe)
Member: Emmanuelle Bouveret
Member: Frédéric Barras
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in PLoS genetics - 01 Nov 2020

Gerstel A, Zamarreño Beas J, Duverger Y, Bouveret E, Barras F, Py B,

Link to Pubmed [PMID] – 33137124

Link to DOI – 10.1371/journal.pgen.1009198

PLoS Genet 2020 Nov; 16(11): e1009198

The level of antibiotic resistance exhibited by bacteria can vary as a function of environmental conditions. Here, we report that phenazine-methosulfate (PMS), a redox-cycling compound (RCC) enhances resistance to fluoroquinolone (FQ) norfloxacin. Genetic analysis showed that E. coli adapts to PMS stress by making Fe-S clusters with the SUF machinery instead of the ISC one. Based upon phenotypic analysis of soxR, acrA, and micF mutants, we showed that PMS antagonizes fluoroquinolone toxicity by SoxR-mediated up-regulation of the AcrAB drug efflux pump. Subsequently, we showed that despite the fact that SoxR could receive its cluster from either ISC or SUF, only SUF is able to sustain efficient SoxR maturation under exposure to prolonged PMS period or high PMS concentrations. This study furthers the idea that Fe-S cluster homeostasis acts as a sensor of environmental conditions, and because its broad influence on cell metabolism, modifies the antibiotic resistance profile of E. coli.