[5] A RACE analysis confirmed that IstR-1 binds TisB mRNA and the duplex is then degraded by RNase III.

[1] 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.

[2] 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.

[4] Also, it has been suggested that TisB may have a role in stabilising the bacterial persistence state after treatment of Escherichia coli with fluoroquinolones.