ArticleNature communications2022
Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
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- Glycerol-Driven Energy and Proteostasis Underpin Antibiotic Tolerance inbioRxiv : the preprint server for biology · 2026Article
- Sculpting Microbial Microenvironments: Spatiotemporal Control via Programmable Electrochemical Gradients.Journal of the American Chemical Society · 2026Review
- Intermittent antibiotic exposure of Escherichia coli biofilms drives resistance in catheter-associated infection models.NPJ biofilms and microbiomes · 2026Article
- The diverse phenotypic and mutational landscape induced by fluoroquinolone treatment.mSystems · 2025Article
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- Hidden Markov Model-Based Prokaryotic Genome Space Mining Reveals the Widespread Pervasiveness of Complex I and Its Potential Evolutionary Scheme.Genome biology and evolution · 2025Article
- Mutations in the Staphylococcus aureus Global Regulator CodY confer tolerance to an interspecies redox-active antimicrobial.PLoS genetics · 2025Article
- Recent Advances in Antimicrobial Resistance: Insights fromMicroorganisms · 2024Review
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- Integrated multi-omics unveil the impact of H-phosphinic analogs of glutamate and α-ketoglutarate on Escherichia coli metabolism.The Journal of biological chemistry · 2024Article
- Metabolic disruption impairs ribosomal protein levels, resulting in enhanced aminoglycoside tolerance.eLife · 2024Article
- Bacterial persisters: molecular mechanisms and therapeutic development.Signal transduction and targeted therapy · 2024Review
- Mutations in thebioRxiv : the preprint server for biology · 2024Article
- METABOLIC DISRUPTION IMPAIRS RIBOSOMAL PROTEIN LEVELS, RESULTING IN ENHANCED AMINOGLYCOSIDE TOLERANCE.bioRxiv : the preprint server for biology · 2024Article
- TisB protein is the single molecular determinant underlying multiple downstream effects of ofloxacin inScience advances · 2024Article
- Article
- Laboratory Evolution of Antimicrobial Resistance in Bacteria to Develop Rational Treatment Strategies.Antibiotics (Basel, Switzerland) · 2024Review
- Exploitation of microbial activities at low pH to enhance planetary health.FEMS microbiology reviews · 2024Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibiotic persistence describes the presence of phenotypic variants within an isogenic bacterial population that are transiently tolerant to antibiotic treatment. Perturbations of metabolic homeostasis can promote antibiotic persistence, but the precise mechanisms are not well understood. Here, we use laboratory evolution, population-wide sequencing and biochemical characterizations to identify mutations in respiratory complex I and discover how they promote persistence in Escherichia coli. We show that persistence-inducing perturbations of metabolic homeostasis are associated with cytoplasmic acidification. Such cytoplasmic acidification is further strengthened by compromised proton pumping in the complex I mutants. While RpoS regulon activation induces persistence in the wild type, the aggravated cytoplasmic acidification in the complex I mutants leads to increased persistence via global shutdown of protein synthesis. Thus, we propose that cytoplasmic acidification, amplified by a compromised complex I, can act as a signaling hub for perturbed metabolic homeostasis in antibiotic persisters.
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