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Where antibiotic resistance mutations meet quorum-sensing.
Rok Krašovec1, Roman V Belavkin2, John A Aston3
1Faculty of Life Sciences, University of Manchester, M13 9PT, UK.
Microbial Cell (Graz, Austria)
|March 31, 2017
Summary
Bacteria can control their mutation rate to antibiotic resistance based on population density. Higher bacterial density leads to a lower mutation rate, a phenomenon termed density-dependent mutation rate plasticity.
Area of Science:
- Microbiology
- Evolutionary Biology
- Genetics
Background:
- Antibiotic resistance is a growing global health crisis.
- The evolution of antibiotic resistance is driven by de novo mutation.
- The rate of mutation may not be constant and could be environmentally regulated.
Purpose of the Study:
- To investigate if bacteria can modulate their mutation rate in response to environmental factors.
- To determine the relationship between bacterial population density and the mutation rate towards antibiotic resistance.
- To explore the underlying mechanisms of this density-dependent mutation rate plasticity.
Main Methods:
- Studied wild-type strains of Escherichia coli in minimal glucose media.
- Assessed mutation rates to rifampicin resistance.
- Correlated mutation rates with bacterial population density and cell-cell interactions.
Main Results:
- Escherichia coli exhibits density-dependent mutation rate plasticity (DD-MRP).
- Mutation rate to rifampicin resistance decreases as bacterial population density increases.
- Cell-cell interactions and population density, not stress levels, influence mutation rate modulation.
Conclusions:
- Bacteria can actively control their mutation rates, specifically towards antibiotic resistance.
- Density-dependent mutation rate plasticity is a novel mechanism influencing microbial evolution.
- The quorum-sensing gene luxS and the activated methyl cycle are implicated in DD-MRP.