Abstract
Bacteria like Escherichia coli employ sensing and gene regulatory systems to respond to stress. The sigma factor RpoS has been shown to play a role in response to stressors like antibiotics. Previous investigations have shown that exposure to a stressor may lead to increased tolerance to a subsequent stressor. This phenomenon, termed cross-protection, has been demonstrated in E. coli, whereby treatment with sub-lethal concentrations of antibiotics delayed T7 bacteriophage-induced lysis. Here we re-examine this cross-protection model and, given its role in the general stress response in E. coli, hypothesize RpoS to be a central mediator of this phenomenon. Using a modified phage lysis assay, we show that delayed T7 phage-induced lysis may not occur in exponential phase cells pretreated with sub-lethal concentrations of ampicillin and gentamicin. In addition, we show that the absence of RpoS does not result in greater susceptibility to T7 phage-induced lysis, suggesting that RpoS may not play a meaningful role in the mediation of cross-protection in exponential phase cells. Along with our results, we propose a complex model of cross-protection, whereby sub-lethal levels of antibiotics, growth phase, stress, and released soluble factors like outer membrane vesicles all play an as-of-yet unclear role in a larger system of bacterial response to stress.