ArticleScientific reports2019
Birth and Resuscitation of (p)ppGpp Induced Antibiotic Tolerant Persister Cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed.
- Seeing Bacterial Persistence Through Different Experimental Lenses: How Methodology Shapes Biological Interpretation.Pathogens (Basel, Switzerland) · 2026Review
- Association ofPathogens (Basel, Switzerland) · 2026Article
- Stringent Response Regulates the Persister Formation and Virulence ofMicroorganisms · 2026Article
- Bacterial Persister Cells as Evolutionary Catalysts of Antibiotic Resistance: Mechanisms, Clinical Implications, and Therapeutic Strategies.Antibiotics (Basel, Switzerland) · 2026Review
- Reduced ROS-associated prophage induction in a lepA mutant contributes to increased fluoroquinolone persistence in Salmonella Typhimurium.Scientific reports · 2026Article
- Beyond metabolic dormancy: metabolic rewiring in bacterial persistence.Nature communications · 2026Review
- Identification of a novel gene inAntimicrobial agents and chemotherapy · 2026Article
- Beyond Resistance: Phenotypic Plasticity in Bacterial Responses to Antibiotics, Oxidative Stress and Antimicrobial Photodynamic Inactivation.Molecules (Basel, Switzerland) · 2026Review
- Sequential eradication of bacterial persisters: integrating phytochemical pharmacology with microenvironment-responsive delivery strategies.Frontiers in microbiology · 2026Review
- Beyond Resistance: Tolerance and Resilience of Bacteria to Photodynamic and Oxidative Stress.International journal of molecular sciences · 2025Review
- Article
- Bioenergetic stress potentiates antimicrobial resistance and persistence.Nature communications · 2025Article
- Observation of persister cell histories reveals diverse modes of survival in antibiotic persistence.eLife · 2025Article
- Type I toxin-antitoxin systems in bacteria: from regulation to biological functions.EcoSal Plus · 2024Review
- The ability in managing reactive oxygen species affectsmSystems · 2024Article
- Bacterial persisters: molecular mechanisms and therapeutic development.Signal transduction and targeted therapy · 2024Review
- The (p)ppGpp synthetase Rsh promotes rifampicin tolerant persister cell formation inFrontiers in microbiology · 2024Article
- Recent Advances in Bacterial Persistence Mechanisms.International journal of molecular sciences · 2023Review
- Environmental conditions define the energetics of bacterial dormancy and its antibiotic susceptibility.Biophysical journal · 2023Article
- Toxin-antitoxin systems in bacterial pathogenesis.Heliyon · 2023Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transient antibiotic treatment typically eradicates most sensitive bacteria except a few survivors called persisters. The second messenger (p)ppGpp plays a key role in persister formation in Escherichia coli populations but the underlying mechanisms have remained elusive. In this study we induced (p)ppGpp synthesis by modulating tRNA charging and then directly observed the stochastic appearance, antibiotic tolerance, and resuscitation of persister cells using live microscopy. Different physiological parameters of persister cells as well as their regularly growing ancestors and sisters were continuously monitored using fluorescent reporters. Our results confirmed previous findings that high (p)ppGpp levels are critical for persister formation, but the phenomenon remained strikingly stochastic without any correlation between (p)ppGpp levels and antibiotic tolerance on the single-cell level. We could not confirm previous notions that persisters exhibit markedly low concentrations of intracellular ATP or were linked to post-transcriptional effects of (p)ppGpp through the activation of small genetic elements known as toxin-antitoxin (TA) modules. Instead, we suggest that persister cell formation under regular conditions is driven by the transcriptional response to increased (p)ppGpp levels.
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