Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell–cell interactions
Year: 2014
Type: article
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.
Source: Nature Communications
DOI: 10.1038/ncomms4742
Language: English
Subfield: Genetics
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $6,990
Awards: G1841899204, SANDPIT: Evolution as an Information Dynamic System, G2761709219, The theory and practice of evolvability: Effects and mechanisms of mutation rate plasticity, G384212634, Uncovering the systems effects of ethanol tolerance evolution in yeast., Uncovering the systems effects of ethanol tolerance evolution in yeast., G8136974013, Functional Object Data Analysis and its Applications
OpenAlex ID: W2145625676
