ReviewmBio2020
A Physiological Basis for Nonheritable Antibiotic Resistance.
Review in mBio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- Single-cell heterogeneity in ribosome levels and protein synthesis during nutrient starvation is driven by cAMP signaling.Science advances · 2026Article
- Bacterial Persister Cells as Evolutionary Catalysts of Antibiotic Resistance: Mechanisms, Clinical Implications, and Therapeutic Strategies.Antibiotics (Basel, Switzerland) · 2026Review
- Study on the Non-Target Metabolomics Effects of Tylosin onVeterinary sciences · 2026Article
- Biomimetic metal-drug coordination nanoplatform to counteract drug resistance in Pseudomonas aeruginosa via energy disruption.Nature communications · 2026Article
- A bacterial toxin-antitoxin system involved in an unusual response to genotoxic stress.EMBO reports · 2025Article
- Enhanced resistance of metal sequestering agents by reconfiguration of the Staphylococcus aureus cell wall.npj antimicrobials and resistance · 2025Article
- Post-fluoroquinolone treatment molecular events and nutrient availability modulatebioRxiv : the preprint server for biology · 2025Article
- Bioenergetic stress potentiates antimicrobial resistance and persistence.Nature communications · 2025Article
- Article
- Cadmium's silent sabotage: unveiling its impact on antibiotic efficacy.Frontiers in microbiology · 2025Article
- Article
- Graphitic Carbon Nitride Confers Bacterial Tolerance to Antibiotics in Wastewater Relating to ATP Depletion.Molecules (Basel, Switzerland) · 2024Article
- Intrinsic antimicrobial resistance: Molecular biomaterials to combat microbial biofilms and bacterial persisters.Biomaterials · 2024Review
- Shaping of microbial phenotypes by trade-offs.Nature communications · 2024Review
- Article
- Basal level of ppGpp coordinatesMicrobial cell (Graz, Austria) · 2023Article
- How Bacterial Pathogens Coordinate Appetite with Virulence.Microbiology and molecular biology reviews : MMBR · 2023Review
- Facially Amphiphilic Bile Acid-Functionalized Antimicrobials: Combating Pathogenic Bacteria, Fungi, and Their Biofilms.ACS infectious diseases · 2023Article
- Influence of Growth Medium Composition on Physiological Responses ofBiotech (Basel (Switzerland)) · 2023Article
- The Capsule Increases Susceptibility to Last-Resort Polymyxins, but Not to Other Antibiotics, in Klebsiella pneumoniae.Antimicrobial agents and chemotherapy · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Antibiotics constitute one of the cornerstones of modern medicine. However, individuals may succumb to a bacterial infection if a pathogen survives exposure to antibiotics. The ability of bacteria to survive bactericidal antibiotics results from genetic changes in the preexisting bacterial genome, from the acquisition of genes from other organisms, and from nonheritable phenomena that give rise to antibiotic tolerance. Nonheritable antibiotic tolerance can be exhibited by a large fraction of the bacterial population or by a small subpopulation referred to as persisters. Nonheritable resistance to antibiotics has been ascribed to the activity of toxins that are part of toxin-antitoxin modules, to the universal energy currency ATP, and to the signaling molecule guanosine (penta) tetraphosphate. However, these molecules are dispensable for nonheritable resistance to antibiotics in many organisms. By contrast, nutrient limitation, treatment with bacteriostatic antibiotics, or expression of genes that slow bacterial growth invariably promote nonheritable resistance. We posit that antibiotic persistence results from conditions promoting feedback inhibition among core cellular processes, resulting phenotypically in a slowdown or halt in bacterial growth.
Indexed as
Identifiers
What OpenQuestion holds
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.