The nine toxin families.

The targets and the types of activities of the nine toxins as well as the cellular processes that are affected by the expression of the toxins are shown. This table is adapted from [7] except where indicated. ND, not determined.1The CcdB toxin does not generate double-strand breaks by itself. Overexpression of CcdB inhibits the re-ligation step of the DNA gyrase, a type II topoisomerase, which leads to the generation of double-strand breaks.2Overexpression of RelE induces cleavage of mRNAs at the ribosome A-site.3,4ParE was shown to poison DNA gyrase and to generate double-strand breaks in vitro.5As CcdB, it induces inhibition of cell division and therefore, it is assumed that it inhibits replication.6Overproduction of the Doc toxin activates the relBE TA system and indirectly causes mRNA cleavage [53].7Doc inhibits translation elongation by association with the 30S ribosomal subunit [54].8See [55]. Although VapC shows an endoribonucleolytic activity, it has not been reported whether or not VapC is able to inhibit translation.9The ζ toxin is part of a three-component TA system (ω−ε−ζ) in which the antitoxin and autoregulation properties are encoded by separate polypeptides.10See [56].11At a high overexpression level, the ζ toxin inhibits replication, transcription, and translation, eventually leading to cell death [57]. However, the specific target(s) is (are) unknown.12See [34].13See [33].14See [32],[33],[34].15The genetic organisation of the higBA system is unusual; the toxin gene is upstream of the antitoxin gene in the operon.16,17See [40],[58].