Where antibiotic resistance mutations meet quorum-sensing
Authors:Rok Krašovec1, Roman V. Belavkin2, John A.D. Aston3, Alastair Channon4, Elizabeth Aston4, Bharat M. Rash1, Manikandan Kadirvel5,6, Sarah Forbes6, and Christopher G. Knight1
doi: 10.15698/mic2014.07.158
Volume 1, pp. 250 to 252, published 25/06/2014.
1 Faculty of Life Sciences, University of Manchester, M13 9PT, UK.
2 School of Science and Technology, Middlesex University, London NW4 4BT, UK.
3 Statistical Laboratory, DPMMS, University of Cambridge, CB3 0WB, UK.
4 Research Institute for the Environment, Physical Sciences and Applied Mathematics, Keele University, ST5 5BG, UK.
5 Wolfson Molecular Imaging Centre, University of Manchester, M20 3LJ, UK.
6 Manchester Pharmacy School, University of Manchester, M13 9PT, UK.
Keywords:
evolution, mutagenesis, fluctuation test, autoinducer 2, autoinducer 3, stress-induced mutagenesis, DNA methylation, optimal control.
Corresponding Author(s):
Conflict of interest statement:
The authors declare that they have no conflicts of interest.
Please cite this article as:
Rok Krašovec, Roman V. Belavkin, John A.D. Aston, Alastair Channon, Elizabeth Aston, Bharat M. Rash, Manikandan Kadirvel, Sarah Forbes, and Christopher G. Knight (2014). Where antibiotic resistance mutations meet quorum-sensing. Microbial Cell 1(7): 250-252.
© 2014 Krašovec 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:
We do not need to rehearse the grim story of the global rise of antibiotic resistant microbes. But what if it were possible to control the rate with which antibiotic resistance evolves by de novo mutation? It seems that some bacteria may already do exactly that: they modify the rate at which they mutate to antibiotic resistance dependent on their biological environment. In our recent study [Krašovec, et al. Nat. Commun. (2014), 5, 3742] we find that this modification depends on the density of the bacterial population and cell-cell interactions (rather than, for instance, the level of stress). Specifically, the wild-type strains of Escherichia coli we used will, in minimal glucose media, modify their rate of mutation to rifampicin resistance according to the density of wild-type cells. Intriguingly, the higher the density, the lower the mutation rate (Figure 1). Why this novel density-dependent ‘mutation rate plasticity’ (DD-MRP) occurs is a question at several levels. Answers are currently fragmentary, but involve the quorum-sensing gene luxS and its role in the activated methyl cycle.