Toxic component of a type I toxin-antitoxin (TA) system (PubMed:18761622) (Probable). Overexpression causes cessation of growth, induces stress-response, a number of membrane protein genes, and leads to cell death (PubMed:15620655, PubMed:18761622, PubMed:18710431). Inhibits ATP synthesis, ATP levels drop drastically quickly after induction (PubMed:18761622, PubMed:24513967). Part of the programmed response to DNA damage; damage leads to increased accumulation of the protein which slows or stops bacterial growth, probably allowing DNA repair before cells continue to grow (PubMed:15620655, PubMed:18761622). Part of the SOS-response regulon, controlled by LexA; repressed by LexA, induced by DNA damage (PubMed:10760155). Antisense sRNA IstR-1 inhibits toxicity by inhibiting translation of tisAB mRNA; subsequent RNase 3 cleavage leads to a truncated mRNA. IstR-1 sequesters a standby ribosome binding site in the tisAB mRNA; as the levels of IstR-1 decrease during the SOS response this site opens and ribosomes are able to bind to initiate translation further downstream (PubMed:15620655, PubMed:17499044). Competition experiments between isogenic strains with or without the tisB/istR-1 region were performed. In the presence of DNA-damaging agents deletion strains were disadvantaged and were almost extinct by 4 days. Originally tisA and tisB were fused into one ORF by frameshift reconstruction. TisA is probably a pseudogene.