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Annu Rev Microbiol. 2012;66:103-23. doi: 10.1146/annurev-micro-092611-150159.

Bacterial persistence and toxin-antitoxin loci.

Author information

1
Center for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, Newcastle University, United Kingdom. Kenn.Gerdes@newcastle.ac.uk

Abstract

Bacterial persistence is caused by the presence of rare, slowly growing bacteria among populations of rapidly growing cells. The slowly growing bacteria are tolerant of antibiotics and other environmental insults, whereas their isogenic, rapidly growing siblings are sensitive. Recent research has shown that persistence of the model organism Escherichia coli depends on toxin-antitoxin (TA) loci. Deletion of type II TA loci reduces the level of persistence significantly. Lon protease but no other known ATP-dependent proteases is required for persistence. Polyphosphate and (p)ppGpp also are required for persistence. These observations led to the proposal of a simple and testable model that explains the persistence of E. coli. It is now important to challenge this model and to test whether the persistence of pathogenic bacteria also depends on TA loci.

[Indexed for MEDLINE]

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