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

KRAŠOVEC, Rok, BELAVKIN, Roman V., ASTON, John A. D., CHANNON, Alastair, ASTON, Elizabeth, RASH, Bharat M., KADIRVEL, Manikandan, FORBES, Sarah and KNIGHT, Christopher G. (2014). Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell–cell interactions. Nature Communications, 5, p. 3742.

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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.

Item Type:	Article
Research Institute, Centre or Group - Does NOT include content added after October 2018:	Biomedical Research Centre
Identification Number:	https://doi.org/10.1038/ncomms4742
Page Range:	p. 3742
Depositing User:	Sarah Forbes
Date Deposited:	03 Jan 2017 15:44
Last Modified:	18 Mar 2021 04:15
URI:	https://shura.shu.ac.uk/id/eprint/14501

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