ArticleNature communications2014
Mutation rate plasticity in rifampicin resistance depends on Escherichia coli cell-cell interactions.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 92 citations in OpenAlex.
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- Adaptive Resistance Mutations at Suprainhibitory Concentrations Independent of SOS Mutagenesis.Molecular biology and evolution · 2021Article
- Inferring environmental transmission using phylodynamics: a case-study using simulated evolution of an enteric pathogen.Journal of the Royal Society, Interface · 2021Article
- Emergent robustness of bacterial quorum sensing in fluid flow.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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9 authors at 4 institutions in 1 country.
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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.
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