Evidence map›Paper›PMID 25874462›Full record

ArticlePLoS pathogens2015

Quadruple quorum-sensing inputs control Vibrio cholerae virulence and maintain system robustness.

Sarah A Jung, Christine A Chapman, Wai-Leung Ng

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
11.1field-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

77 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Deployment of amBio · 2025
    Article
  6. Quorum sensing regulates virulence factors in the coral pathogenApplied and environmental microbiology · 2025
    Article
  7. Deployment of abioRxiv : the preprint server for biology · 2024
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Small regulatory RNAs inmicroLife · 2023
    Review
  14. Intestinal colonization againstAIMS microbiology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Sequence Polymorphisms inApplied and environmental microbiology · 2022
    Article
  19. Review
  20. Article

17 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Sarah A JungDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America; Program in Molecular Microbiology, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America.
Christine A ChapmanDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Wai-Leung NgDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America; Program in Molecular Microbiology, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America.
Tufts University · US

Funding

MOLECULAR ANALYSIS OF MICROBIAL PATHOGENST32AI007422 · NIAID · TUFTS UNIVERSITY BOSTON · PI Ralph R. Isberg · 1992 to 2026
$5.7M
NIAID NIH HHS T32 AI007422NIAID NIH HHS T32AI007422
6 · The paper itself

Abstract

Bacteria use quorum sensing (QS) for cell-cell communication to carry out group behaviors. This intercellular signaling process relies on cell density-dependent production and detection of chemical signals called autoinducers (AIs). Vibrio cholerae, the causative agent of cholera, detects two AIs, CAI-1 and AI-2, with two histidine kinases, CqsS and LuxQ, respectively, to control biofilm formation and virulence factor production. At low cell density, these two signal receptors function in parallel to activate the key regulator LuxO, which is essential for virulence of this pathogen. At high cell density, binding of AIs to their respective receptors leads to deactivation of LuxO and repression of virulence factor production. However, mutants lacking CqsS and LuxQ maintain a normal LuxO activation level and remain virulent, suggesting that LuxO is activated by additional, unidentified signaling pathways. Here we show that two other histidine kinases, CqsR (formerly known as VC1831) and VpsS, act upstream in the central QS circuit of V. cholerae to activate LuxO. V. cholerae strains expressing any one of these four receptors are QS proficient and capable of colonizing animal hosts. In contrast, mutants lacking all four receptors are phenotypically identical to LuxO-defective mutants. Importantly, these four functionally redundant receptors act together to prevent premature induction of a QS response caused by signal perturbations. We suggest that the V. cholerae QS circuit is composed of quadruple sensory inputs and has evolved to be refractory to sporadic AI level perturbations.

Indexed as

AnimalsCholeraGene Expression Regulation, BacterialLuminescent MeasurementsMiceQuorum SensingVibrio choleraeVirulence

Identifiers

PMID25874462
PMCPMC4398556
OpenAlexW2086474106

What OpenQuestion holds

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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.