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Bacterial toxin-antitoxin systems: more than selfish entities?

Van Melderen L, Saavedra De Bast M - PLoS Genet. (2009)

Bottom Line: They are composed of closely linked genes encoding a stable toxin that can harm the host cell and its cognate labile antitoxin, which protects the host from the toxin's deleterious effect.This Review discusses current hypotheses regarding the biological roles of these evolutionarily successful small operons.We consider the various selective forces that could drive the maintenance of TA systems in bacterial genomes.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire de Génétique et Physiologie Bactérienne, IBMM, Faculté des Sciences, Université Libre de Bruxelles, Gosselies, Belgium.

ABSTRACT
Bacterial toxin-antitoxin (TA) systems are diverse and widespread in the prokaryotic kingdom. They are composed of closely linked genes encoding a stable toxin that can harm the host cell and its cognate labile antitoxin, which protects the host from the toxin's deleterious effect. TA systems are thought to invade bacterial genomes through horizontal gene transfer. Some TA systems might behave as selfish elements and favour their own maintenance at the expense of their host. As a consequence, they may contribute to the maintenance of plasmids or genomic islands, such as super-integrons, by post-segregational killing of the cell that loses these genes and so suffers the stable toxin's destructive effect. The function of the chromosomally encoded TA systems is less clear and still open to debate. This Review discusses current hypotheses regarding the biological roles of these evolutionarily successful small operons. We consider the various selective forces that could drive the maintenance of TA systems in bacterial genomes.

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Related in: MedlinePlus

The anti-addiction model.The chromosomally encoded anti-addiction system is represented in black; the PSK+ plasmid in purple. In this model, the antitoxin of the chromosomally encoded TA system is able to counteract the toxin of the plasmid-encoded system. Therefore, daughter bacteria that do not inherit a plasmid copy at cell division will survive post-segregational killing.
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pgen-1000437-g002: The anti-addiction model.The chromosomally encoded anti-addiction system is represented in black; the PSK+ plasmid in purple. In this model, the antitoxin of the chromosomally encoded TA system is able to counteract the toxin of the plasmid-encoded system. Therefore, daughter bacteria that do not inherit a plasmid copy at cell division will survive post-segregational killing.

Mentions: The anti-addiction model proposes that chromosomally-encoded systems can selectively advantage their host in post-segregational killing conditions. In theory, chromosomally-encoded antitoxins sharing sufficient identity with homologous plasmid-encoded TA systems might act as anti-addiction modules by preventing post-segregational killing (Figure 2). The ccdEch chromosomally encoded TA system of Erwinia chrysanthemi 3937 was shown to have this property with respect to its E. coli F plasmid–encoded ccdF homolog [43]. In an E. coli strain containing the ccdEch system inserted in its chromosome (ccdEch strain), no post-segregational killing was observed upon the loss of a plasmid carrying ccdF. Moreover, competition experiments showed that under post-segregational killing conditions, the ccdEch strain had a selective advantage compared to the wild-type strain. Therefore, the fitness advantage conferred by the newly acquired anti-addiction module under post-segregational killing conditions might allow its fixation in the bacterial population. In turn, the plasmid-encoded system will lose its addictive character. On the one hand, variants able to evade anti-addiction modules are expected to be selected and out-compete their post-segregational killing–defective relatives. Anti-addiction might thus be one of the evolutionary forces driving selection of the plasmid encoded TA systems. On the other hand, chromosomally encoded TA systems might lose their anti-addictive properties [10] and decay [44].


Bacterial toxin-antitoxin systems: more than selfish entities?

Van Melderen L, Saavedra De Bast M - PLoS Genet. (2009)

The anti-addiction model.The chromosomally encoded anti-addiction system is represented in black; the PSK+ plasmid in purple. In this model, the antitoxin of the chromosomally encoded TA system is able to counteract the toxin of the plasmid-encoded system. Therefore, daughter bacteria that do not inherit a plasmid copy at cell division will survive post-segregational killing.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2654758&req=5

pgen-1000437-g002: The anti-addiction model.The chromosomally encoded anti-addiction system is represented in black; the PSK+ plasmid in purple. In this model, the antitoxin of the chromosomally encoded TA system is able to counteract the toxin of the plasmid-encoded system. Therefore, daughter bacteria that do not inherit a plasmid copy at cell division will survive post-segregational killing.
Mentions: The anti-addiction model proposes that chromosomally-encoded systems can selectively advantage their host in post-segregational killing conditions. In theory, chromosomally-encoded antitoxins sharing sufficient identity with homologous plasmid-encoded TA systems might act as anti-addiction modules by preventing post-segregational killing (Figure 2). The ccdEch chromosomally encoded TA system of Erwinia chrysanthemi 3937 was shown to have this property with respect to its E. coli F plasmid–encoded ccdF homolog [43]. In an E. coli strain containing the ccdEch system inserted in its chromosome (ccdEch strain), no post-segregational killing was observed upon the loss of a plasmid carrying ccdF. Moreover, competition experiments showed that under post-segregational killing conditions, the ccdEch strain had a selective advantage compared to the wild-type strain. Therefore, the fitness advantage conferred by the newly acquired anti-addiction module under post-segregational killing conditions might allow its fixation in the bacterial population. In turn, the plasmid-encoded system will lose its addictive character. On the one hand, variants able to evade anti-addiction modules are expected to be selected and out-compete their post-segregational killing–defective relatives. Anti-addiction might thus be one of the evolutionary forces driving selection of the plasmid encoded TA systems. On the other hand, chromosomally encoded TA systems might lose their anti-addictive properties [10] and decay [44].

Bottom Line: They are composed of closely linked genes encoding a stable toxin that can harm the host cell and its cognate labile antitoxin, which protects the host from the toxin's deleterious effect.This Review discusses current hypotheses regarding the biological roles of these evolutionarily successful small operons.We consider the various selective forces that could drive the maintenance of TA systems in bacterial genomes.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire de Génétique et Physiologie Bactérienne, IBMM, Faculté des Sciences, Université Libre de Bruxelles, Gosselies, Belgium.

ABSTRACT
Bacterial toxin-antitoxin (TA) systems are diverse and widespread in the prokaryotic kingdom. They are composed of closely linked genes encoding a stable toxin that can harm the host cell and its cognate labile antitoxin, which protects the host from the toxin's deleterious effect. TA systems are thought to invade bacterial genomes through horizontal gene transfer. Some TA systems might behave as selfish elements and favour their own maintenance at the expense of their host. As a consequence, they may contribute to the maintenance of plasmids or genomic islands, such as super-integrons, by post-segregational killing of the cell that loses these genes and so suffers the stable toxin's destructive effect. The function of the chromosomally encoded TA systems is less clear and still open to debate. This Review discusses current hypotheses regarding the biological roles of these evolutionarily successful small operons. We consider the various selective forces that could drive the maintenance of TA systems in bacterial genomes.

Show MeSH
Related in: MedlinePlus