ArticleCell systems2017
Regulatory Dynamics Determine Cell Fate following Abrupt Antibiotic Exposure.
Article in Cell systems, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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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.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Suppression of bacterial cell death underlies the antagonistic interaction between ciprofloxacin and tetracycline.Molecular systems biology · 2026Article
- Single-cell heterogeneity underpins antagonistic antibiotic interactions.Molecular systems biology · 2026Article
- Drug delivery dynamics dictate evolution of bacterial antibiotic responses.The ISME journal · 2025Article
- Harnessing CRISPR interference to resensitize laboratory strains and clinical isolates to last resort antibiotics.Scientific reports · 2025Article
- Dynamics of drug delivery determines course of evolution of antibiotic responses in bacteria.bioRxiv : the preprint server for biology · 2024Article
- Common regulatory mutation increases single-cell survival to antibiotic exposures inbioRxiv : the preprint server for biology · 2024Article
- Dynamical model of antibiotic responses linking expression of resistance genes to metabolism explains emergence of heterogeneity during drug exposures.Physical biology · 2024Article
- Optimal transcriptional regulation of dynamic bacterial responses to sudden drug exposures.Biophysical journal · 2022Article
- Nutrient Gradients Mediate Complex Colony-Level Antibiotic Responses in Structured Microbial Populations.Frontiers in microbiology · 2022Article
- Antibiotic Persistence as a Metabolic Adaptation: Stress, Metabolism, the Host, and New Directions.Pharmaceuticals (Basel, Switzerland) · 2018Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Bacterial resistance mechanisms must cope with transient fast-changing conditions. These systems are often repressed in the absence of the drug, and it is unclear how their regulation can provide a quick response when challenged. Here, we focus on the tet operon, which provides resistance to tetracycline through efflux pump TetA. We show that, somewhat counterintuitively, prompt expression of the TetA repressor TetR is key for cellular survival upon abrupt drug exposure. Tracking individual cells upon exposure, we find that differences in the rate of TetR elevation result in three distinct cell fates: recovery (high rate), death due to excess TetA (intermediate rate), and death from the drug (low rate). A surge of TetR expression optimizes the response by allowing sensitive detection of both the initial rise and the later decline of intracellular drug, avoiding an undesirable overshoot in TetA expression. These results show how regulatory circuits of resistance genes have evolved for optimized dynamics.
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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.