The toxin-antitoxin systemtisB-istR1

Ménage à trois

“…4B), an arrangement that is also observed in other Enterobacteriaceae 70 , 71 . Intriguingly, both promoters start transcription at the same nucleotide, thus preventing the generation of GlmY species with altered 5′−ends, 70 which may lead to functionally different variants as observed for sRNAs IstR1 and IstR2 73 . Although such an overlapping σ 54 /σ 70 promoter architecture was never observed before, more recent studies indicate that it may also apply to other genes 74 .…”

Bacterial type I toxin-antitoxin systems

“…14 Kawano suggests that bacteria benefit from TA systems in their defense against invasion factors like bacteriophages. 9 As Wagner and Unoson emphasize in this issue, 13 it has been found only recently that chromosomal TA systems play a role in persister formation. 15,16 Persister cells are a subset of a bacterial population that has stochastically entered a dormant state and thus becomes refractory to the action of antibiotics, whereas their isogenic, rapidly growing siblings are sensitive.…”

“…The IstR1 RNA binds 100 nt upstream of the tisB translation initiation region (TIR) at an unstructured ribosome standby-site, thereby restraining ribosomes from binding there and sliding into the TIR when the stem-loop region opens up occasionally. 13 Interestingly, the antitoxin RNA II of the E. faecalis plasmid pAD combines features of cis-and trans-encoded sRNAs: Toxin and antitoxin RNA overlap by a bidirectional terminator (similar to cis-encoded antisense RNAs) and, additionally, contain a set of direct repeat sequences located far apart (like trans-encoded antisense RNAs). RNAII/fst RNA binding yields a partial duplex, which is sufficient to block fst translation.…”

“…9 Similarly, only one of three tisB mRNA variants derived from 5' endonucleolytic processing is translated. 13 Sometimes, the toxin gene is only transcribed under certain conditions: tisB and symE are under SOS control, i.e., regulated by the Lex repressor. Proteolytic digestion by Lon protease affects SymE levels.…”

“…In some cases, RNase III is essential for the action of the antitoxin (txpA/RatA, yonT/As-yonT), whereas in others (hok/Sok, symE/ SymR, ibs/Sib, tisB/IstRI and bsrG/SR4) it is dispensable. 7,9,13,14 Although toxin inhibition by the RNA antitoxin is the major regulatory principle, various additional strategies are employed by type I TA systems to guarantee tight regulation of toxin expression or to keep toxin levels low unless they are required. In many cases, the toxin SD sequence is sequestered by intramolecular base-pairing (tisB, shoB, bsrG, txpA) that obstructs ribosome binding, and the start codon of yonT is GUG, which also likely reduces translation initiation.…”