A multistress responsive type I toxin-antitoxin system: bsrE/SR5 from the B. subtilis chromosome.

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.

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

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 5' 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 Vitro Characterization of the Type I Toxin-Antitoxin System bsrE/SR5 from Bacillus subtilis.

BsrE/SR5 is a new type I toxin/antitoxin system located on the prophage-like region P6 of the Bacillus subtilis chromosome. The bsrE gene encoding a 30-amino acid hydrophobic toxin and the antitoxin gene sr5 overlap at their 3' ends by 112 bp. Overexpression of bsrE causes cell lysis on agar plates.

Against the mainstream: the membrane-associated type I toxin BsrG from Bacillus subtilis interferes with cell envelope biosynthesis without increasing membrane permeability.

Toxin-antitoxin loci, which encode a toxic protein alongside with either RNA or a protein able to counteract the toxicity, are widespread among archaea and bacteria. These loci are implicated in persistence, and as addiction modules to ensure stable inheritance of plasmids and phages. In type I toxin-antitoxin systems, a small RNA acts as an antitoxin, which prevents the synthesis of the toxin.

sRNAs in bacterial type I and type III toxin-antitoxin systems.

Toxin-antitoxin (TA) loci consist of two genes: a stable toxin whose overexpression kills the cell or causes growth stasis and an unstable antitoxin that neutralizes the toxin action. Currently, five TA systems are known. Here, we review type I and type III systems in which the antitoxins are regulatory RNAs.

One antitoxin--two functions: SR4 controls toxin mRNA decay and translation.

Type I toxin-antitoxin systems encoded on bacterial chromosomes became the focus of research during the past years. However, little is known in terms of structural requirements, kinetics of interaction with their targets and regulatory mechanisms of the antitoxin RNAs. Here, we present a combined in vitro and in vivo analysis of the bsrG/SR4 type I toxin-antitoxin system from Bacillus subtilis.

Type I toxin-antitoxin systems in Bacillus subtilis.

Type I toxin-antitoxin (TA) systems are widespread in bacteria and consist of a toxin-encoding mRNA and a partially overlapping antisense RNA that blocks expression of the toxin, either at the level of translation or by mRNA degradation. Four type I toxin families have so far been proposed in B. subtilis based on sequence similarity: TxpA/BsrG, BsrH/BsrE, YonT and YhzE and two (TxpA and BsrG) have been studied in some detail.

BsrG/SR4 from Bacillus subtilis--the first temperature-dependent type I toxin-antitoxin system.

Here, we describe bsrG/SR4, a novel type I toxin-antitoxin system from the SPβ prophage region of the Bacillus subtilis chromosome. The 294-nucleotide bsrG RNA encodes a 38-amino-acid toxin, whereas SR4 is a 180-nucleotide antisense RNA that acts as the antitoxin. Both genes overlap by 123 nucleotides.