ArticleNature microbiology2016
Frequency of antibiotic application drives rapid evolutionary adaptation of Escherichia coli persistence.
Article in Nature microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
147 citing papers in PubMed, 279 citations in OpenAlex.
- Exogenous indole promotes florfenicol tolerance inVirulence · 2026Article
- Population size modulates the transition from gene amplification-mediated heteroresistance to stable resistance.npj antimicrobials and resistance · 2026Article
- Collateral sensitivity-harnessing microbial vulnerabilities as a solution to antimicrobial resistance.Molecular biology reports · 2026Review
- Article
- Selective context, rather than persister cycling alone, drives resistance fixation in Escherichia coli.npj antimicrobials and resistance · 2026Article
- High-throughput protocol for assessing antibiotic resistance using agar dilution, acoustic liquid handling, and semi-automated image analysis.STAR protocols · 2026Article
- Bacterial Persistence Modulates the Speed, Magnitude, and Onset of Antibiotic Resistance Evolution.Molecular biology and evolution · 2026Article
- Genome-wide screen reveals a universal role of ATP in ciprofloxacin tolerance among genetically distinctmLife · 2026Article
- Single-cell analysis reveals critical toxin/antitoxin ratio triggering persister resuscitation.Molecular systems biology · 2026Article
- Linkage-aware inference of fitness from short-read time-series genomic data.bioRxiv : the preprint server for biology · 2026Article
- Linkage-aware inference of fitness from short-read time-series genomic data.Virus evolution · 2026Article
- A side-effect-free chemotactic-antibacterial wound dressing for programmatic trapping, killing of bacteria, and wound repair.Materials today. Bio · 2025Article
- Phenotypic heterogeneity in lag reflects an evolutionarily stable bet-hedging strategy.bioRxiv : the preprint server for biology · 2025Article
- Increased Expression of AbcA Efflux Pump Accelerated Resistance Development from Tolerance to Resistance Against Oxacillin inMicroorganisms · 2025Article
- Surviving Colonies ofAntibiotics (Basel, Switzerland) · 2025Article
- Systematic design of pulse dosing to eradicate persister bacteria: The case of fluoroquinolones.Computers & chemical engineering · 2025Article
- Experimental evolution ofMicrobiology spectrum · 2025Article
- Enhanced diagnosis of multi-drug-resistant microbes using group association modeling and machine learning.Nature communications · 2025Article
- Priestia megaterium cells are primed for surviving lethal doses of antibiotics and chemical stress.Communications biology · 2025Article
- Drug delivery dynamics dictate evolution of bacterial antibiotic responses.The ISME journal · 2025Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The evolution of antibiotic resistance is a major threat to society and has been predicted to lead to 10 million casualties annually by 2050(1). Further aggravating the problem, multidrug tolerance in bacteria not only relies on the build-up of resistance mutations, but also on some cells epigenetically switching to a non-growing antibiotic-tolerant 'persister' state(2-6). Yet, despite its importance, we know little of how persistence evolves in the face of antibiotic treatment(7). Our evolution experiments in Escherichia coli demonstrate that extremely high levels of multidrug tolerance (20-100%) are achieved by single point mutations in one of several genes and readily emerge under conditions approximating clinical, once-daily dosing schemes. In contrast, reversion to low persistence in the absence of antibiotic treatment is relatively slow and only partially effective. Moreover, and in support of previous mathematical models(8-10), we show that bacterial persistence quickly adapts to drug treatment frequency and that the observed rates of switching to the persister state can be understood in the context of 'bet-hedging' theory. We conclude that persistence is a major component of the evolutionary response to antibiotics that urgently needs to be considered in both diagnostic testing and treatment design in the battle against multidrug tolerance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.