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

Author

Listed:
  • Rok Krašovec

    (Faculty of Life Sciences, The University of Manchester, Michael Smith Building)

  • Roman V. Belavkin

    (School of Science and Technology, Middlesex University)

  • John A. D. Aston

    (Statistical Laboratory, DPMMS, University of Cambridge
    University of Warwick)

  • Alastair Channon

    (Research Institute for the Environment, Physical Sciences and Applied Mathematics, Keele University)

  • Elizabeth Aston

    (Research Institute for the Environment, Physical Sciences and Applied Mathematics, Keele University)

  • Bharat M. Rash

    (Faculty of Life Sciences, The University of Manchester, Michael Smith Building)

  • Manikandan Kadirvel

    (Wolfson Molecular Imaging Centre, The University of Manchester
    Manchester Pharmacy School, The University of Manchester)

  • Sarah Forbes

    (Manchester Pharmacy School, The University of Manchester)

  • Christopher G. Knight

    (Faculty of Life Sciences, The University of Manchester, Michael Smith Building)

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.

Suggested Citation

  • Rok Krašovec & Roman V. Belavkin & John A. D. Aston & Alastair Channon & Elizabeth Aston & Bharat M. Rash & Manikandan Kadirvel & Sarah Forbes & Christopher G. Knight, 2014. "Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell–cell interactions," Nature Communications, Nature, vol. 5(1), pages 1-8, September.
  • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4742
    DOI: 10.1038/ncomms4742
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