ArticleScientific reports2018
Access to high-impact mutations constrains the evolution of antibiotic resistance in soft agar.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Exploring molecular mechanisms of aminoglycoside resistance in Escherichia coli MG1655 using the antibiotic resistance growth plate.Scientific reports · 2026Article
- Two complementingRNA biology · 2025Article
- Sequential antibiotic exposure restores antibiotic susceptibility.The Journal of antimicrobial chemotherapy · 2025Article
- Selective silencing of antibiotic-tethered ribosomes as a resistance mechanism against aminoglycosides.Nature communications · 2025Article
- Tripartite Loops Reverse Antibiotic Resistance.Molecular biology and evolution · 2025Article
- In Vitro Resistance-Predicting Studies and In Vitro Resistance-Related Parameters-A Hit-to-Lead Perspective.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Beta-lactamase dependent and independent evolutionary paths to high-level ampicillin resistance.Nature communications · 2024Article
- Fitness Costs of Antibiotic Resistance Impede the Evolution of Resistance to Other Antibiotics.ACS infectious diseases · 2023Article
- Emergence of ResistantFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite widespread resistance to many important antibiotics, the factors that govern the emergence and prevalence of antibiotic-resistant bacteria are still unclear. When exposed to antibiotic gradients in soft agar plates measuring as little as 1.25 × 11 cm we found that Escherichia coli rapidly became resistant to representatives from every class of antibiotics active against Gram-negative bacteria. Evolution kinetics were independent of the frequency of spontaneous mutations that confer antibiotic resistance or antibiotic dose-response curves, and were only loosely correlated to maximal antibiotic concentrations. Instead, rapid evolution required unrealized mutations that could markedly decrease antibiotic susceptibility. When bacteria could not evolve through these "high-impact" mutations, populations frequently bottlenecked, reducing the number of cells from which mutants could arise and prolonging evolution times. This effect was independent of the antibiotic's mechanism of action, and may affect the evolution of antibiotic resistance in clinical settings.
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