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. 2012 Mar 13;7(3):e32199. doi: 10.1371/journal.pone.0032199

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Cline et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) During colonization under favourable conditions, the VapBC-1 complex binds to and autorepresses TA operon transcription. (B) Stress induces Lon and Clp proteases that degrade VapB-1, releasing active VapC-1 toxin. (C) The ribonuclease activity of VapC-1 facilitates a state of bacteriostasis, resulting in nonspecific antibiotic tolerance. (D) Upon improved conditions, Fis activates vapBC-1 operon transcription, displacing any bound VapC-1. Fis levels decrease in early exponential growth, allowing the VapBC-1 complex to bind and restore transcriptional equilibrium.