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.
Bibliographical noteFunding Information:
We thank Richard A. Lenski and Karina B. Xavier for strains; and Casey M. Bergman, Michael A. Brockhurst, Andrew J. McBain, R. Craig Maclean, Chris Simms and Dan P. Smith for discussions and critical readings of the manuscript. This work was supported by Engineering and Physical Sciences Research Council (EPSRC) grant EP/H031936/1 and Biotechnology and Biological Sciences Research Council (BBSRC) grant BB/L009579/1. C.G.K. was supported by fellowship 082453/Z/07/Z from the Wellcome Trust.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Physics and Astronomy(all)