Elevated Expression of Toxin TisB Protects Persister Cells against Ciprofloxacin but Enhances Susceptibility to Mitomycin C

摘要: Bacterial chromosomes harbor toxin-antitoxin (TA) systems, some of which are implicated in the formation multidrug-tolerant persister cells. In Escherichia coli, toxin TisB from tisB/istR-1 TA system depolarizes inner membrane and causes ATP depletion, presumably favors formation. Transcription tisB is induced upon DNA damage due to activation SOS response by LexA degradation. Transcriptional counteracted on post-transcriptional level structural features mRNA RNA antitoxin IstR-1. Deletion regulatory elements (mutant Δ1-41 ΔistR) uncouples expression LexA-dependent induction a ‘high persistence’ (hip) phenotype treatment with different antibiotics. Here, we demonstrate use fluorescent reporters that overexpression mutant ΔistR inhibits cellular processes, including genes. The failure gene does not affect hip fluoroquinolone ciprofloxacin, likely because depletion avoids strong damage. By contrast, cells highly susceptible cross-linker mitomycin C, SOS-dependent repair systems impeded. Hence, conditional strongly depends DNA-damaging agent.