Evidence map›Paper›PMID 24780952›Full record

ArticlePloS one2014

A gacS deletion in Pseudomonas aeruginosa cystic fibrosis isolate CHA shapes its virulence.

Khady Mayebine Sall, Maria Guillermina Casabona, Christophe Bordi, Philippe Huber, Sophie de Bentzmann, Ina Attrée, Sylvie Elsen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. EPY001, a Novel Monoclonal Antibody AgainstInternational journal of molecular sciences · 2025
    Article
  3. Review
  4. The role of theFrontiers in cellular and infection microbiology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. The Evanescent GacS Signal.Microorganisms · 2020
    Review
  9. Article
  10. Article
  11. Frontiers in immunology · 2018
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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 6 institutions in 1 country.

Khady Mayebine SallINSERM, UMR-S 1036, Biology of Cancer and Infection, Grenoble, France; CNRS, ERL 5261, Bacterial Pathogenesis and Cellular Responses, Grenoble, France; UJF-Grenoble 1, Grenoble, France; CEA, DSV/iRTSV, Grenoble, France.
Maria Guillermina CasabonaINSERM, UMR-S 1036, Biology of Cancer and Infection, Grenoble, France; CNRS, ERL 5261, Bacterial Pathogenesis and Cellular Responses, Grenoble, France; UJF-Grenoble 1, Grenoble, France; CEA, DSV/iRTSV, Grenoble, France.
Christophe BordiLaboratoire d'Ingénierie des Systèmes Macromoléculaires, UMR 7255 CNRS - Aix Marseille University, Marseille, France.
Philippe HuberINSERM, UMR-S 1036, Biology of Cancer and Infection, Grenoble, France; CNRS, ERL 5261, Bacterial Pathogenesis and Cellular Responses, Grenoble, France; UJF-Grenoble 1, Grenoble, France; CEA, DSV/iRTSV, Grenoble, France.
Sophie de BentzmannLaboratoire d'Ingénierie des Systèmes Macromoléculaires, UMR 7255 CNRS - Aix Marseille University, Marseille, France.
Ina AttréeINSERM, UMR-S 1036, Biology of Cancer and Infection, Grenoble, France; CNRS, ERL 5261, Bacterial Pathogenesis and Cellular Responses, Grenoble, France; UJF-Grenoble 1, Grenoble, France; CEA, DSV/iRTSV, Grenoble, France.
Sylvie ElsenINSERM, UMR-S 1036, Biology of Cancer and Infection, Grenoble, France; CNRS, ERL 5261, Bacterial Pathogenesis and Cellular Responses, Grenoble, France; UJF-Grenoble 1, Grenoble, France; CEA, DSV/iRTSV, Grenoble, France.
Commissariat à l'Énergie Atomique et aux Énergies Alternatives · FRAix-Marseille Université · FRCentre National de la Recherche Scientifique · FRInstitut de Recherches en Technologies et Sciences pour le Vivant · FRPathogénèse Bactérienne et Réponses CellulairesUniversité Grenoble Alpes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa, a human opportunistic pathogen, is capable of provoking acute and chronic infections that are associated with defined sets of virulence factors. During chronic infections, the bacterium accumulates mutations that silence some and activate other genes. Here we show that the cystic fibrosis isolate CHA exhibits a unique virulence phenotype featuring a mucoid morphology, an active Type III Secretion System (T3SS, hallmark of acute infections), and no Type VI Secretion System (H1-T6SS). This virulence profile is due to a 426 bp deletion in the 3' end of the gacS gene encoding an essential regulatory protein. The absence of GacS disturbs the Gac/Rsm pathway leading to depletion of the small regulatory RNAs RsmY/RsmZ and, in consequence, to expression of T3SS, while switching off the expression of H1-T6SS and Pel polysaccharides. The CHA isolate also exhibits full ability to swim and twitch, due to active flagellum and Type IVa pili. Thus, unlike the classical scheme of balance between virulence factors, clinical strains may adapt to a local niche by expressing both alginate exopolysaccharide, a hallmark of membrane stress that protects from antibiotic action, host defences and phagocytosis, and efficient T3S machinery that is considered as an aggressive virulence factor.

Indexed as

Gene DeletionGenes, BacterialAmino Acid SequenceBacterial ProteinsBiofilmsCystic FibrosisMolecular Sequence DataPolymerase Chain ReactionPseudomonas aeruginosaSequence Homology, Amino AcidVirulenceBacterial Proteins

Identifiers

PMID24780952
PMCPMC4004566
OpenAlexW2078848565

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.