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Journal of Bacteriology, July 2008, p. 4603-4609, Vol. 190, No. 13
0021-9193/08/$08.00+0 doi:10.1128/JB.00357-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Laboratoire de Génétique et Physiologie Bactérienne, Institut de Biologie et Médecine Moléculaires, Université Libre de Bruxelles, 12 rue des Professeurs Jeener et Brachet, B : 6041 Gosselies, Belgium
Received 11 March 2008/ Accepted 11 April 2008
Toxin-antitoxin (TA) systems are widespread among bacterial chromosomes and mobile genetic elements. Although in plasmids TA systems have a clear role in their vertical inheritance by selectively killing plasmid-free daughter cells (postsegregational killing or addiction phenomenon), the physiological role of chromosomally encoded ones remains under debate. The assumption that chromosomally encoded TA systems are part of stress response networks and/or programmed cell death machinery has been called into question recently by the observation that none of the five canonical chromosomally encoded TA systems in the Escherichia coli chromosome seem to confer any selective advantage under stressful conditions (V. Tsilibaris, G. Maenhaut-Michel, N. Mine, and L. Van Melderen, J. Bacteriol. 189:6101-6108, 2007). Their prevalence in bacterial chromosomes indicates that they might have been acquired through horizontal gene transfer. Once integrated in chromosomes, they might in turn interfere with their homologues encoded by mobile genetic elements. In this work, we show that the chromosomally encoded Erwinia chrysanthemi ccd (control of cell death) (ccdEch) system indeed protects the cell against postsegregational killing mediated by its F-plasmid ccd (ccdF) homologue. Moreover, competition experiments have shown that this system confers a fitness advantage under postsegregational conditions mediated by the ccdF system. We propose that ccdEch acts as an antiaddiction module and, more generally, that the integration of TA systems in bacterial chromosomes could drive the evolution of plasmid-encoded ones and select toxins that are no longer recognized by the antiaddiction module.
Published ahead of print on 25 April 2008.
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