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Bacteria encounter sub-inhibitory concentrations of antibiotics in various niches, where these low doses play a key role for antibiotic resistance selection. However, the physiological effects of these sub-lethal concentrations and their observed connection to the cellular mechanisms generating genetic diversification are still poorly understood. It is known that, unlike for the model bacterium  Escherichia coli , sub-minimal inhibitory concentrations (sub-MIC) of aminoglycosides (AGs) induce the SOS response in  Vibrio cholerae . SOS is induced upon DNA damage, and since AGs do not directly target DNA, we addressed two issues in this study: how sub-MIC AGs induce SOS in  V. cholerae  and why they do not do so in  E. coli . We found that when bacteria are grown with tobramycin at a concentration 100-fold below the MIC, intracellular reactive oxygen species strongly increase in  V. cholerae  but not in  E. coli . Using flow cytometry and  gfp  fusions with the SOS regulated promoter of  intIA , we followed AG-dependent SOS induction. Testing the different mutation repair pathways, we found that over-expression of the base excision repair (BER) pathway protein MutY relieved this SOS induction in  V. cholerae , suggesting a role for oxidized guanine in AG-mediated indirect DNA damage. As a corollary, we established that a BER pathway deficient  E. coli  strain induces SOS in response to sub-MIC AGs. We finally demonstrate that the RpoS general stress regulator prevents oxidative stress-mediated DNA damage formation in  E. coli . We further show that AG-mediated SOS induction is conserved among the distantly related Gram negative pathogens  Klebsiella pneumoniae  and  Photorhabdus luminescens , suggesting that  E. coli  is more of an exception than a paradigm for the physiological response to antibiotics sub-MIC.

RpoS Plays a Central Role in the SOS Induction by Sub-Lethal Aminoglycoside Concentrations in Vibrio cholerae