Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell-cell interactions

Channon, A

doi:10.1038/ncomms4742

Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell-cell interactions

Channon, A

Authors

Alastair Channon a.d.channon@keele.ac.uk

Abstract

Variation of mutation rate at a particular site in a particular genotype, in other words mutation rate plasticity (MRP), can be caused by stress or ageing. However, mutation rate control by other factors is less well characterized. Here we show that in wild-type Escherichia coli (K-12 and B strains), the mutation rate to rifampicin resistance is plastic and inversely related to population density: lowering density can increase mutation rates at least threefold. This MRP is genetically switchable, dependent on the quorum-sensing gene luxS--specifically its role in the activated methyl cycle--and is socially mediated via cell-cell interactions. Although we identify an inverse association of mutation rate with fitness under some circumstances, we find no functional link with stress-induced mutagenesis. Our experimental manipulation of mutation rates via the social environment raises the possibility that such manipulation occurs in nature and could be exploited medically.

Acceptance Date	Mar 27, 2014
Publication Date	Apr 29, 2014
Journal	Nature Communications
Print ISSN	2041-1723
Pages	3742 -?
DOI	https://doi.org/10.1038/ncomms4742
Keywords	Analysis of Variance, Bacterial Proteins, Carbon-Sulfur Lyases, DNA Primers, Drug Resistance, Bacterial, Escherichia coli, Genetic Fitness, Genetic Variation, Microbial Interactions, Mutation Rate, Population Density, Real-Time Polymerase Chain Reaction,