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Where antibiotic resistance mutations meet quorum-sensing

Channon

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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.

Citation

Channon. (2014). Where antibiotic resistance mutations meet quorum-sensing. Microbial Cell, 250 - 252. https://doi.org/10.15698/mic2014.07.158

Acceptance Date Jun 16, 2014
Publication Date Jun 25, 2014
Journal Microbial Cell
Publisher Shared Science Publishers
Pages 250 - 252
DOI https://doi.org/10.15698/mic2014.07.158
Keywords evolution, mutagenesis, fluctuation test, autoinducer 2, autoinducer 3, stress-induced mutagenesis, DNA methylation, optimal control
Publisher URL https://doi.org/10.15698/mic2014.07.158

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