Bacterial type I toxin-antitoxin systems

Brantl, Sabine

doi:10.4161/rna.23045

Cited by 66 publications

(75 citation statements)

References 16 publications

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“…RatA, its cognate antitoxin was characterized as an asRNA. 4,5 Regulatory model at the TAI-II locus The cis-organization of mazEF and txpA-ratA modules, ensures a coordinated expression of the TAI-II locus featuring i) controls previously known for individual TAs in other species, 12,[48][49][50] and ii) a regulatory interplay relying on drm sequences and the mazEFdependent transcriptional activation of ratA (Fig. 7).…”

Section: Discussionmentioning

confidence: 99%

Regulatory crosstalk between type I and type II toxin-antitoxin systems in the human pathogen Enterococcus faecalis

et al. 2015

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We discovered a chromosomal locus containing 2 toxin-antitoxin modules (TAs) with an antisense transcriptional organization in the E. faecalis clinical isolate V583. These TAs are homologous to the type I txpA-ratA system and the type II mazEF, respectively. We have shown that the putative MazF is toxic for E. coli and triggers RNA degradation, and its cognate antitoxin MazE counteracts toxicity. The second module, adjacent to mazEF, expresses a toxin predicted to belong to the TxpA type I family found in Firmicutes, and the antisense RNA antidote, RatA. Genomic analysis indicates that the cis-association of mazEF and txpA-ratA modules has been favored during evolution, suggesting a selective advantage for this TA organization in the E. faecalis species. We showed regulatory interplays between the 2 modules, involving transcription control and RNA stability. Remarkably, our data reveal that MazE and MazEF have a dual transcriptional activity: they act as autorepressors and activate ratA transcription, most likely in a direct manner. RatA controls txpA RNA levels through stability. Our data suggest a pivotal role of MazEF in the coordinated expression of mazEF and txpA-ratA modules in V583. To our knowledge, this is the first report describing a crosstalk between type I and II TAs.

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Section: Discussionmentioning

confidence: 99%

Regulatory crosstalk between type I and type II toxin-antitoxin systems in the human pathogen Enterococcus faecalis

et al. 2015

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“…in refs. 3,4 ). Whereas in type I and III TA systems, the antitoxin is a small RNA, in type II, IV and V systems toxin and antitoxin are proteins.…”

Section: Introductionmentioning

confidence: 99%

A multistress responsive type I toxin-antitoxin system:bsrE/SR5 from theB. subtilischromosome

et al. 2016

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bsrE/SR5 is a type I TA system from prophage-like element P6 of the B. subtilis chromosome. The 256 nt bsrE RNA encodes a 30 aa toxin. The antitoxin SR5 is a 163 nt antisense RNA. Both genes overlap at their 3 0 ends. Overexpression of bsrE causes cell lysis on agar plates, which can be neutralized by sr5 overexpression, whereas deletion of the chromosomal sr5 copy has no effect. SR5 is short-lived with a halflife of 7 min, whereas bsrE RNA is stable with a half-life of >80 min. The sr5 promoter is 10-fold stronger than the bsrE promoter. SR5 interacts with the 3 0 UTR of bsrE RNA, thereby promoting its degradation by recruiting RNase III. RNase J1 is the main RNase responsible for SR5 and bsrE RNA degradation, and PnpA processes an SR5 precursor to the mature RNA. Hfq stabilizes SR5, but is not required for its inhibitory function. While bsrE RNA is affected by temperature shock and alkaline stress, the amount of SR5 is significantly influenced by various stresses, among them pH, anoxia and iron limitation. Only the latter one is dependent on sigB. Both RNAs are extremely unstable upon ethanol stress due to rapid degradation by RNase Y.

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“…Currently, five types of toxin-antitoxin (TA) systems are known (reviewed by Brantl, 2012b). In type I TA modules, RNA antitoxins are small regulatory RNAs that inhibit expression of convergently or divergently transcribed toxin mRNAs by base-pairing interactions.…”

Section: Introductionmentioning

confidence: 99%

Heat-shock-induced refolding entails rapid degradation of bsrG toxin mRNA by RNases Y and J1

Jahn

Brantl

2016

Microbiology

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Gene regulation accomplished by alternative folding of an mRNA is a widely used mechanism. Classical examples are the various transcriptional attenuation mechanisms that employ, for example, leader peptide translation, or binding of a modified protein, an uncharged tRNA or an antisense RNA to the 59 untranslated region of an mRNA. With the discovery of transcriptional and translational riboswitches, it became clear that small metabolites or even metal ions can also alter RNA secondary structures and, hence, gene expression. In addition, biophysical factors like temperature can affect RNA folding, as exemplified by RNA thermometers. We have investigated in detail the type I toxin-antitoxin system bsrG/SR4 from Bacillus subtilis. The antitoxin SR4 is a cis-encoded regulatory RNA that neutralizes BsrG toxin action. SR4 prevents toxin expression by promoting degradation of the toxin mRNA and inhibiting its translation. In addition, upon temperature shock the amount of toxin mRNA decreases significantly. Here, we demonstrate that heat shock induces a refolding in the central region of the toxin mRNA that makes it more accessible to degradation by RNases Y and J1. Furthermore, we show that BsrG might play a role at the onset of stationary phase, when the antitoxin SR4 can no longer prevent toxin synthesis.

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Bacterial type I toxin-antitoxin systems

Cited by 66 publications

References 16 publications

Regulatory crosstalk between type I and type II toxin-antitoxin systems in the human pathogen Enterococcus faecalis

Regulatory crosstalk between type I and type II toxin-antitoxin systems in the human pathogen Enterococcus faecalis

A multistress responsive type I toxin-antitoxin system:bsrE/SR5 from theB. subtilischromosome

Heat-shock-induced refolding entails rapid degradation of bsrG toxin mRNA by RNases Y and J1

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