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

Channon, A

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.

Citation

Channon, A. (2014). Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell-cell interactions. Nature communications, 3742 -?. https://doi.org/10.1038/ncomms4742

• Acceptance Date: Mar 27, 2014
• Publication Date: Apr 29, 2014
• Journal: Nature Communications
• Print ISSN: 2041-1723
• Pages: 3742 -?
• DOI: https://doi.org/10.1038/ncomms4742
• Keywords: Analysis of Variance, Bacterial Proteins, Carbon-Sulfur Lyases, DNA Primers, Drug Resistance, Bacterial, Escherichia coli, Genetic Fitness, Genetic Variation, Microbial Interactions, Mutation Rate, Population Density, Real-Time Polymerase Chain Reaction, Rifampin