Krasovec, R, Belavkin, RV, Aston, JAD, Channon, AD ORCID: https://orcid.org/0000-0001-9224-4931, Aston, E, Rash, BM, Kadirvel, M, Forbes, S and Knight, CG (2014) Where antibiotic resistance mutations meet quorum-sensing. Microbial Cell, 1 (7). 250 - 252.

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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.

Item Type: Article
Uncontrolled Keywords: evolution, mutagenesis, fluctuation test, autoinducer 2, autoinducer 3, stress-induced mutagenesis, DNA methylation, optimal control
Subjects: Q Science > QA Mathematics > QA75 Electronic computers. Computer science
Divisions: Faculty of Natural Sciences > School of Computing and Maths
Depositing User: Symplectic
Date Deposited: 22 Jun 2015 15:32
Last Modified: 15 Mar 2019 16:43
URI: http://eprints.keele.ac.uk/id/eprint/601

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