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
Download full text from publisher
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4742. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.