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Nat Commun. 2014 Apr 29;5:3742. doi: 10.1038/ncomms4742.

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

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Faculty of Life Sciences, The University of Manchester, Michael Smith Building, Manchester M13 9PT, UK.
School of Science and Technology, Middlesex University, London NW4 4BT, UK.
1] Statistical Laboratory, DPMMS, University of Cambridge, Cambridge CB3 0WB, UK [2] Department of Statistics, University of Warwick, Warwick CV4 7AL, UK.
Research Institute for the Environment, Physical Sciences and Applied Mathematics, Keele University, Keele ST5 5BG, UK.
1] Wolfson Molecular Imaging Centre, The University of Manchester, Manchester M20 3LJ, UK [2] Manchester Pharmacy School, The University of Manchester, Manchester M13 9PT, UK.
Manchester Pharmacy School, The University of Manchester, Manchester M13 9PT, UK.


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.

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