Abstract
The diversity of Type-II toxin–antitoxin (TA) systems in bacterial genomes requires tightly controlled interaction specificity to ensure protection of the cell, and potentially to limit cross-talk between toxin–antitoxin pairs of the same family of TA systems. Further, there is a redundant use of toxin folds for different cellular targets and complexation with different classes of antitoxins, increasing the apparent requirement for the insulation of interactions. The presence of Type II TA systems has remained enigmatic with respect to potential benefits imparted to the host cells. In some cases, they play clear roles in survival associated with unfavorable growth conditions. More generally, they can also serve as a “cure” against acquisition of highly similar TA systems such as those found on plasmids or invading genetic elements that frequently carry virulence and resistance genes. The latter model is predicated on the ability of these highly specific cognate antitoxin–toxin interactions to form cross-reactions between chromosomal antitoxins and invading toxins. This review summarizes advances in the Type II TA system models with an emphasis on antitoxin cross-reactivity, including with invading genetic elements and cases where toxin proteins share a common fold yet interact with different families of antitoxins.
Highlights
Toxin–antitoxin (TA) systems are abundant in bacterial and archaeal chromosomes as well as extra-chromosomal genetic elements including plasmids, phages, and transposons [1,2,3,4,5,6,7]
The VapC-type toxins found in M. tuberculosis, Shigella flexneri and Rickettsia felis have minor variations in numbers of specific secondary structure elements [167,168]
TA systems are abundant on bacterial chromosomes with a seemingly high insulation from non-homologous interactions
Summary
Toxin–antitoxin (TA) systems are abundant in bacterial and archaeal chromosomes as well as extra-chromosomal genetic elements including plasmids, phages, and transposons [1,2,3,4,5,6,7]. TA systems have been the subject of numerous reviews that describe their typically bicistronic operon encoding a toxin that targets essential cellular process and the cognate neutralizing antitoxin [8,9,10,11,12,13,14,15,16]. Depending on the molecular identity of the antitoxin, as well as the mechanism by which it neutralizes the toxin, the known TA systems have been classified into six different types. In Type II systems the antitoxin partner plays a dual role by neutralizing the cognate toxin and by mediating transcriptional regulation bindinginto its promoter, identified [35,36,37]. 2. Paradigms for Type II TA Systems acetylation of antitoxins and/or chaperone protection [44,45,46], in addition to widespread variations on the bicistronic antitoxin–toxin arrangement [44,47]. Analysis of xenolog regulation through bindingthat to its promoter, making lynchpin of Type
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