Toxin-Antitoxin Systems

An additional mechanism which plasmids use to favor their maintenance in bacte­rial populations involves the killing or growth impairment of cells that fail to acquire a copy of the plasmid. This has variously been referred to as postsegregational cell killing, plasmid addiction, or toxin-antitoxin systems (57-60). This mechanism involves a plasmid-encoded protein toxin and antitoxin. The antitoxin, which may be either a protein or a nontranslated RNA, neutralizes the toxin by either binding to the toxin protein or by inhibiting its translation. The antitoxin is more susceptible to degradation by host enzymes than the toxin and, thus, replenishment of the antitoxin levels by the presence of plasmid is required to prevent toxin action. When a plas-mid-free derivative arises (e.g., as a result of a replication or partitioning defect), the toxin is subsequently liberated to interact with an intracellular target and cause either death or a growth disadvantage of the plasmid-free cell (see Fig. 4). In the case of the CcdAB toxin-antitoxin system encoded by the F plasmid, the toxin (CcdB) is a DNA gyrase poison. It both entraps a cleavage