Evidence map›Paper›PMID 33875652›Full record

ArticleNature communications2021

Cytoplasmic condensation induced by membrane damage is associated with antibiotic lethality.

Felix Wong, Jonathan M Stokes, Bernardo Cervantes, Sider Penkov, Jens Friedrichs, Lars D Renner, James J Collins

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
13.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  5. Differential survival and tolerance mechanisms ofApplied and environmental microbiology · 2026
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  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Antibiotic-Induced Bacterial Cell Death: A "Radical" Way of Dying?Current topics in microbiology and immunology · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Eating a way out of antibiotics.Nature chemical biology · 2025
    Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Felix WongInstitute for Medical Engineering & Science and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-2309-8835
Jonathan M StokesInstitute for Medical Engineering & Science and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Bernardo CervantesInstitute for Medical Engineering & Science and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Sider PenkovInstitute for Clinical Chemistry and Laboratory Medicine at the University Clinic and Medical Faculty of TU Dresden, Dresden, Germany.
Jens FriedrichsLeibniz Institute of Polymer Research and the Max Bergmann Center of Biomaterials, Dresden, Germany.
Lars D RennerLeibniz Institute of Polymer Research and the Max Bergmann Center of Biomaterials, Dresden, Germany. renner@ipfdd.de.ORCID 0000-0003-0178-1788
James J CollinsInstitute for Medical Engineering & Science and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. jimjc@mit.edu.ORCID 0000-0002-5560-8246
Broad Institute · USLeibniz Institute of Polymer Research · DEMax Bergmann Zentrum für Biomaterialien · DETechnische Universität Dresden · DE

Funding

Genetic, Metabolic and Regulatory Control of MIC and Relapse in M. tuberculosisR01AI146194 · NIAID · UNIVERSITY OF WASHINGTON · PI ALLAND, DAVID, SHERMAN, DAVID R · 2020 to 2024
$4.1M
NIAID NIH HHS R01 AI146194
6 · The paper itself

Abstract

Bactericidal antibiotics kill bacteria by perturbing various cellular targets and processes. Disruption of the primary antibiotic-binding partner induces a cascade of molecular events, leading to overproduction of reactive metabolic by-products. It remains unclear, however, how these molecular events contribute to bacterial cell death. Here, we take a single-cell physical biology approach to probe antibiotic function. We show that aminoglycosides and fluoroquinolones induce cytoplasmic condensation through membrane damage and subsequent outflow of cytoplasmic contents as part of their lethality. A quantitative model of membrane damage and cytoplasmic leakage indicates that a small number of nanometer-scale membrane defects in a single bacterium can give rise to the cellular-scale phenotype of cytoplasmic condensation. Furthermore, cytoplasmic condensation is associated with the accumulation of reactive metabolic by-products and lipid peroxidation, and pretreatment of cells with the antioxidant glutathione attenuates cytoplasmic condensation and cell death. Our work expands our understanding of the downstream molecular events that are associated with antibiotic lethality, revealing cytoplasmic condensation as a phenotypic feature of antibiotic-induced bacterial cell death.

Indexed as

AminoglycosidesAnti-Bacterial AgentsCell MembraneCell Membrane PermeabilityCytoplasmEscherichia coliFluoroquinolonesMicrobial Sensitivity TestsMicrobial ViabilityMicroscopy, Atomic ForceMicroscopy, FluorescenceSingle-Cell AnalysisAminoglycosidesAnti-Bacterial AgentsFluoroquinolones

Identifiers

PMID33875652
PMCPMC8055701
OpenAlexW3153738948

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.