ArticleNature communications2020
Highly parallel lab evolution reveals that epistasis can curb the evolution of antibiotic resistance.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 82 citations in OpenAlex.
- Predicting resistance evolution to guide antibiotic development.Nature reviews. Microbiology · 2026Review
- Non-canonical gene amplifications facilitate adaptive evolution in bacteria.Nature microbiology · 2026Article
- Simultaneous optimization of lignocellulosic sugar catabolism via systematic laboratory evolution under complex selection pressure.Nature communications · 2026Article
- Function-specific epistasis shapes evolutionary trajectories towards antibiotic resistance.Nature communications · 2026Article
- Epistasis and co-adaptation in bacterial genome evolution.Nature reviews. Genetics · 2026Review
- Resistance potentiators: Evolutionary catalysts of antibiotic resistance.PLoS biology · 2026Article
- Co-targeting Metabolic Neighbours Constraints Bacterial Adaptive Evolution.bioRxiv : the preprint server for biology · 2026Article
- Proteostasis-targeted antibacterial strategies.Journal of microbiology (Seoul, Korea) · 2026Review
- Evolutionary drivers of divergent collateral sensitivity responses during antibiotic therapy.Nature ecology & evolution · 2026Review
- Historical contingency limits adaptive diversification in a spatially structured environment.Evolution letters · 2026Article
- Macrolide resistance trajectories across threeFrontiers in microbiology · 2026Article
- Experimental evolution in an era of molecular manipulation.Nature reviews. Genetics · 2026Review
- Unraveling Epistatic Interactions Between Sites Under Drug-Dependent Selection in the Mycobacterium tuberculosis Genome.Molecular biology and evolution · 2025Article
- Impeding pathways of intrinsic resistance in Escherichia coli confers antibiotic sensitization and resistance proofing.PLoS biology · 2025Article
- Evolution under vancomycin selection drives divergent collateral sensitivity patterns inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Idiosyncratic evolvability among single-point ribosomal mutants towards multi-aminoglycoside resistance.PLoS genetics · 2025Article
- Strategies and efforts in circumventing the emergence of antiviral resistance against conventional antivirals.npj antimicrobials and resistance · 2025Review
- Quantitative analysis of relationship between mutation rate and speed of adaptation under antibiotic exposure in Escherichia coli.PLoS genetics · 2025Article
- Mechanisms of antimicrobial resistance: From genetic evolution to clinical manifestations.AIMS microbiology · 2025Review
- From Petri Dishes to Patients to Populations: Scales and Evolutionary Mechanisms Driving Antibiotic Resistance.Annual review of microbiology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
Genetic perturbations that affect bacterial resistance to antibiotics have been characterized genome-wide, but how do such perturbations interact with subsequent evolutionary adaptation to the drug? Here, we show that strong epistasis between resistance mutations and systematically identified genes can be exploited to control spontaneous resistance evolution. We evolved hundreds of Escherichia coli K-12 mutant populations in parallel, using a robotic platform that tightly controls population size and selection pressure. We find a global diminishing-returns epistasis pattern: strains that are initially more sensitive generally undergo larger resistance gains. However, some gene deletion strains deviate from this general trend and curtail the evolvability of resistance, including deletions of genes for membrane transport, LPS biosynthesis, and chaperones. Deletions of efflux pump genes force evolution on inferior mutational paths, not explored in the wild type, and some of these essentially block resistance evolution. This effect is due to strong negative epistasis with resistance mutations. The identified genes and cellular functions provide potential targets for development of adjuvants that may block spontaneous resistance evolution when combined with antibiotics.
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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.