ArticlePLoS genetics2013
Elevated mutagenesis does not explain the increased frequency of antibiotic resistant mutants in starved aging colonies.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Consideration of a Liquid Mutation-Accumulation Experiment to Measure Mutation Rates by Successive Serial Dilution.Genome biology and evolution · 2025Article
- Stress-resistant but phage-sensitive host mutants induced by phage T4 ghost adsorption.Frontiers in microbiology · 2025Article
- Cultivating antimicrobial resistance: how intensive agriculture ploughs the way for antibiotic resistance.Microbiology (Reading, England) · 2023Review
- Adaptive Resistance Mutations at Suprainhibitory Concentrations Independent of SOS Mutagenesis.Molecular biology and evolution · 2021Article
- DNA Breaks-Mediated Fitness Cost Reveals RNase HI as a New Target for Selectively Eliminating Antibiotic-Resistant Bacteria.Molecular biology and evolution · 2021Article
- Radial Expansion Facilitates the Maintenance of Double Antibiotic Resistances.Antimicrobial agents and chemotherapy · 2020Article
- Rapid cell division of Staphylococcus aureus during colonization of the human nose.BMC genomics · 2019Article
- Fitness of Spontaneous Rifampicin-ResistantFrontiers in microbiology · 2019Article
- The Codon Usage of Lowly Expressed Genes Is Subject to Natural Selection.Genome biology and evolution · 2018Article
- Evolution of Antibiotic Resistance without Antibiotic Exposure.Antimicrobial agents and chemotherapy · 2017Article
- Rapid Genetic Adaptation during the First Four Months of Survival under Resource Exhaustion.Molecular biology and evolution · 2017Article
- A shifting mutational landscape in 6 nutritional states: Stress-induced mutagenesis as a series of distinct stress input-mutation output relationships.PLoS biology · 2017Article
- Molecular and cellular bases of adaptation to a changing environment in microorganisms.Proceedings. Biological sciences · 2016Review
- Mutation--The Engine of Evolution: Studying Mutation and Its Role in the Evolution of Bacteria.Cold Spring Harbor perspectives in biology · 2015Review
- Alarmingly High Segregation Frequencies of Quinolone Resistance Alleles within Human and Animal Microbiomes Are Not Explained by Direct Clinical Antibiotic Exposure.Genome biology and evolution · 2015Article
- Stress-induced mutation rates show a sigmoidal and saturable increase due to the RpoS sigma factor in Escherichia coli.Genetics · 2014Article
- Stress-induced mutagenesis and complex adaptation.Proceedings. Biological sciences · 2014Article
- The impact of drug resistance on Mycobacterium tuberculosis physiology: what can we learn from rifampicin?Emerging microbes & infections · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The frequency of mutants resistant to the antibiotic rifampicin has been shown to increase in aging (starved), compared to young colonies of Escherichia coli. These increases in resistance frequency occur in the absence of any antibiotic exposure, and similar increases have also been observed in response to additional growth limiting conditions. Understanding the causes of such increases in the frequency of resistance is important for understanding the dynamics of antibiotic resistance emergence and spread. Increased frequency of rifampicin resistant mutants in aging colonies is cited widely as evidence of stress-induced mutagenesis (SIM), a mechanism thought to allow bacteria to increase mutation rates upon exposure to growth-limiting stresses. At the same time it has been demonstrated that some rifampicin resistant mutants are relatively fitter in aging compared to young colonies, indicating that natural selection may also contribute to increased frequency of rifampicin resistance in aging colonies. Here, we demonstrate that the frequency of mutants resistant to both rifampicin and an additional antibiotic (nalidixic-acid) significantly increases in aging compared to young colonies of a lab strain of Escherichia coli. We then use whole genome sequencing to demonstrate conclusively that SIM cannot explain the observed magnitude of increased frequency of resistance to these two antibiotics. We further demonstrate that, as was previously shown for rifampicin resistance mutations, mutations conferring nalidixic acid resistance can also increase fitness in aging compared to young colonies. Our results show that increases in the frequency of antibiotic resistant mutants in aging colonies cannot be seen as evidence of SIM. Furthermore, they demonstrate that natural selection likely contributes to increases in the frequency of certain antibiotic resistance mutations, even when no selection is exerted due to the presence of antibiotics.
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