by RNase III. Degradation results in a +106 form, an inactive 249 nt transcript which cannot be translated. Proposed function of the IstR-TisB toxin-antitoxin system The proposed function of this toxin-antitoxin system is to cause growth arrest, rather than cell death, in response to DNA damage, allowing time for repair processes to occur. TisB translation is under LexA control, so it is induced by DNA damage as part of the SOS response. Under normal conditions, very little tisB mRNA is synthesised and translation is inhibited, but when DNA damage occurs tisAB is strongly induced causing overexpression, which overrides inhibition by depleting the IstR-1 pool. Experimental data has shown effects of TisB to be decreases in transcription, translation and replication, RNA degradation and ribosome disassembly. TisB does not affect transcription and translation directly in vitro, so these effects are thought to be downstream consequences of membrane damage. TisB insertion into the membrane is thought to result in a loss of membrane potential. This could account for a decrease in ATP concentration in cells following triggering of the SOS response, causing slowing of cellular processes and inhibited cell growth. See also Toxin-antitoxin system Sib RNA hok/sok system References Further reading External links EcoCyc page for Istr-1 EcoliWiki page for TisB Antisense RNA RNA antitoxins Toxins