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. 2014 Jan 10;6(1):304–324. doi: 10.3390/toxins6010304

Figure 1.

Figure 1

The addiction phenomenon. Toxin-antitoxin (TA) systems participate in plasmid maintenance in growing bacterial populations by a mechanism called addiction or post-segregational killing. Addiction relies on the differential stability of the toxin and antitoxin. A: Daughter-bacteria that inherit a plasmid copy encoding the ccd (control of cell death) toxin-antitoxin system grow normally. B: Daughter-bacteria that do not inherit a plasmid copy still have antitoxin-toxin complexes in their cytoplasm. C: The CcdA antitoxin (light green) is degraded by the Lon protease, while the CcdB toxin (dark green) is stable. CcdB is, therefore, liberated from the CcdA-CcdB complex and is able to interact with DNA-gyrase, a class II topoisomerase. The interaction of CcdB with DNA-gyrase inhibits DNA replication and leads eventually to cell death. Addiction leads to the selective killing of plasmid-free daughter bacteria and increases plasmid prevalence in the bacterial population.