The anion-selective, small, pore-forming, multistate, persister-promoting toxin, TisB (Gurnev et al., 2012; Steinbrecher et al., 2012). It forms a transmembrane amphipathic α-helix with all charged and hydrophilic residues on one side of the helix. TisB is activated in response to DNA damage or by ciprofloxacin exposure, often involving the SOS response and promotes persister formation in a manner similar to HokB (TC# 1.E.53.1.3; Harms et al. 2016). TisB protects Escherichia coli cells suffering massive DNA damage from environmental toxic compounds (Su et al. 2022).  Toxin/antitoxin (TA) modules are involved in persister formation in E.coli. The SOS response leads to overexpression of TisB and persister formation. TisB is a membrane-acting peptide that apparently sends cells into dormancy by decreasing the proton motive force and ATP levels (Lewis 2010). Protein aggregation is a consequence of the dormancy-inducing membrane toxin TisB in E. coli (Leinberger et al. 2024). TisB is the single molecular determinant underlying multiple downstream effects of ofloxacin in E. coli (Cayron et al. 2024).