Membrane depolarization-triggered responsive diversification leads to antibiotic tolerance

Authors:

Natalie Verstraeten, Wouter Joris Knapen, Maarten Fauvart, Jan Michiels

doi: 10.15698/mic2015.08.220
Volume 2, pp. 299 to 301, published 24/07/2015.

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Affiliations:

Centre of Microbial and Plant Genetics, KU Leuven – University of Leuven, 3001 Leuven, Belgium.

Keywords: 

Obg, ObgE, CgtA, YhbZ, persistence, antibiotic tolerance, (p)ppGpp, HokB, toxin antitoxin, responsive diversification, membrane depolarization.

Corresponding Author(s):

Jan Michiels, Centre of Microbial and Plant Genetics, Department of Microbial and Molecular Systems, KU Leuven - University of Leuven; Kasteelpark Arenberg 20 box 2460, 3001 Leuven, Belgium Jan.Michiels@biw.kuleuven.be

Conflict of interest statement:

The authors declare no conflict of interest.

Please cite this article as:

Natalie Verstraeten, Wouter Joris Knapen, Maarten Fauvart, Jan Michiels (2015). Membrane depolarization-triggered responsive diversification leads to antibiotic tolerance. Microbial Cell 2(8): 299-301.

© 2015 Verstraeten et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

Bacterial populations are known to harbor a small fraction of so-called persister cells that have the remarkable ability to survive treatment with very high doses of antibiotics. Recent studies underscore the importance of persistence in chronic infections, yet the nature of persisters remains poorly understood. We recently showed that the universally conserved GTPase Obg modulates persistence via a (p)ppGpp-dependent mechanism that proceeds through expression of hokB. HokB is a membrane-bound toxin that causes the membrane potential to collapse. The resulting drop in cellular energy levels triggers a switch to the persistent state, yielding protection from antibiotic attack. Obg-mediated persistence is conserved in the human pathogen Pseudomonas aeruginosa, making Obg a promising target for therapies directed against bacterial persistence.