Abstract
Toxin–antitoxin (TA) systems were originally discovered as plasmid maintenance systems in a multitude of free-living bacteria, but were afterwards found to also be widespread in bacterial chromosomes. TA loci comprise two genes, one coding for a stable toxin whose overexpression kills the cell or causes growth stasis, and the other coding for an unstable antitoxin that counteracts toxin action. Of the currently known six types of TA systems, in Bacillus subtilis, so far only type I and type II TA systems were found, all encoded on the chromosome. Here, we review our present knowledge of these systems, the mechanisms of antitoxin and toxin action, and the regulation of their expression, and we discuss their evolution and possible physiological role.
Highlights
Toxin–antitoxin (TA) systems are genetic modules that are widespread in bacterial genomes and plasmids
We provide an overview of the known B. subtilis TA systems with special focus on their molecular mechanisms, the control of toxin and antitoxin expression, the modes of toxin action, and their biological role
In the B. subtilis type I TA systems studied so far, the RNA antitoxins bind at the 30 end of the toxin messenger RNAs (mRNAs) and support their degradation
Summary
Toxin–antitoxin (TA) systems are genetic modules that are widespread in bacterial genomes and plasmids They consist of a gene pair encoding a stable toxin that impedes cell growth by interfering with fundamental processes, and an unstable antitoxin that counteracts the toxin activity. In type I TA systems, antitoxins interact with the corresponding toxin messenger RNAs (mRNAs) [1]. In type III systems, the RNA antitoxin binds the toxin protein directly. Antitoxins in type IV TA systems interfere with binding of the toxin proteins to their cellular targets [2]. We provide an overview of the known B. subtilis TA systems with special focus on their molecular mechanisms, the control of toxin and antitoxin expression, the modes of toxin action, and their biological role
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