Vloga proteina TisB pri zaščiti bakterije Escherichia coli pred kolicinom E7 in bakteriofagom T4

Bacteria use various strategies to survive in stressful environments. In Escherichia coli (E. coli), DNA damage caused by antibiotics such as trimethoprim (TMP) and mitomycin C (MMC) triggers the SOS response, which activates the tisB gene. The TisB protein is a small toxin that damages the cell membrane and reduces the proton motive force (PMF), which affects bacterial survival and how cells respond to their environment. This thesis investigates how TisB affects the survival of E. coli after treatment with TMP or MMC, its role in defence against colicin E7, and its effect on infection with bacteriophage T4. Wild-type (WT) and ∆tisB strains were compared by measuring survival under varying concentrations of MMC or TMP, the extent of membrane depolarisation, and survival outcomes in environments with the colicin E7-producing strain BZB2110. The results show that TisB-induced depolarisation affects survival in an antibiotic-dependent manner and can either protect against colicin E7 by reducing membrane transport, or limit the import of nutrients necessary for survival. In addition, the effect of TisB on bacteriophage T4 infection was examined by measuring burst size with and without prior SOS induction, and the ∆tisB strain exhibited larger burst sizes compared to the WT strain. However, this difference may be due to other factors and is not necessarily a consequence of lower viral entry into depolarised WT cells. The results obtained provide a better understanding of the complexity of bacterial defence systems and their role in survival in competitive environments.