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

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