TisB Protein Protects Escherichia coli Cells Suffering Massive DNA Damage from Environmental Toxic Compounds
Wei-Lin Su, Marie-Florence Bredèche, Sara Dion, Julie Dauverd, Bénédicte Condamine, Arnaud Gutierrez, Érick Denamur, Ivan Matić
Abstract
The contribution of toxin-antitoxin systems to the persistence of bacteria to antibiotics has been intensively studied. This is also the case with the E. coli TisB/IstR toxin-antitoxin system, but the contribution of TisB to the persistence to antibiotics turned out to be not as straightforward as anticipated. In this study, we show that TisB can decrease, but also increase, cytotoxicity of different antibiotics. This inconsistency has a common origin, i.e., TisB-induced collapse of the PMF, which impacts the import and the action of different antibiotics. By taking into account the natural habitat of TisB bacterial hosts, the facts that this toxin-antitoxin system is integrated into the genotoxic stress response regulon SOS and that both SOS regulon and TisB are required for E. coli to colonize the host intestine, and the phenotypic consequences of the collapse of the PMF, we propose that TisB protects its hosts from cytotoxic molecules produced by competing intestinal bacteria.