Sublethal Concentrations of Antibiotics Do Not Markedly Delay T7 Bacteriophage-Mediated Lysis Between Wild-Type and rpoS, and oxyR Mutants of Escherichia coli

SUMMARY T7 bacteriophages are obligatory lytic phages that infect bacterial cells, and hijack host cell machinery to replicate their genome. Bacteriophage infection acts as an environmental stressor for E. coli, like other known factors such as antibiotics, and nutrient deprivation. In response to stressors, E. coli has been shown to increase the production of the regulatory proteins RpoS and OxyR. Both regulators may play a role in protective response against oxidative stress, which is induced by exposure to sublethal antibiotic concentrations. Previous studies have suggested that increased production of RpoS and OxyR following sublethal concentration of antibiotics may play an important role in delaying T7 bacteriophage-mediated cell lysis. However, this cross-protection phenomenon is not well understood. The aim of our project is to investigate the role of RpoS and OxyR in delaying T7 bacteriophage-mediated cell lysis following exposure to sublethal antibiotic concentrations by comparing the onset of lysis in E. coli wild-type (WT) strains to that of rpoS and oxyR single knockout mutant strains. We hypothesized that both RpoS and OxyR are necessary for the delayed T7 bacteriophage-mediated cell lysis in E. coli strain BW25113 following exposure to sublethal antibiotic concentrations. Validation of each strain was achieved via PCR and sublethal concentrations of ampicillin, gentamicin, and kanamycin were determined using a minimum inhibitory concentration (MIC) assay. Infectivity assay of the two mutant E. coli strains treated with a range of sublethal antibiotic concentrations did not show a change in the onset or the rate of lysis compared to the WT.