Evidence map›Paper›PMID 15385461›Full record

ArticleInfection and immunity2004

Pseudomonas aeruginosa relA contributes to virulence in Drosophila melanogaster.

David L Erickson, J Louise Lines, Everett C Pesci, Vittorio Venturi, Douglas G Storey

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

63 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. c-di-GMP is a key regulator of Pseudomonas aeruginosa response to UVA radiation.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
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  3. Within-host adaptation mutations associated with persistent colonization ofFrontiers in cellular and infection microbiology · 2026
    Article
  4. Article
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  7. Infection and immunity · 2023
    Review
  8. Article
  9. Mutating bothFrontiers in microbiology · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Frontiers in cellular and infection microbiology · 2020
    Review
  20. Article

3 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

5 authors at 3 institutions in 3 countries.

David L EricksonDepartment of Biological Sciences, University of Calgary, Alberta, Canada.
J Louise Lines
Everett C Pesci
Vittorio Venturi
Douglas G Storey
East Carolina University · USInternational Centre for Genetic Engineering and Biotechnology · ITUniversity of Calgary · CA

Funding

ROLE OF A NEW SIGNAL MOLECULE IN P. AERUGINOSA VIRULENCER01AI046682 · NIAID · EAST CAROLINA UNIVERSITY · PI PESCI, EVERETT C · 2000 to 2004
$1.2M
NIAID NIH HHS R01 AI046682NIAID NIH HHS R01-AI46682
6 · The paper itself

Abstract

The stringent response is a mechanism by which bacteria adapt to nutritional deficiencies through the production of the guanine nucleotides ppGpp and pppGpp, produced by the RelA enzyme. We investigated the role of the relA gene in the ability of an extracellular pathogen, Pseudomonas aeruginosa, to cause infection. Strains lacking the relA gene were created from the prototypical laboratory strain PAO1 as well as the mucoid cystic fibrosis isolate 6106, which lacks functional quorum-sensing systems. The absence of relA abolished the production of ppGpp and pppGpp under conditions of amino acid starvation. We found that strains lacking relA exhibited reduced virulence in a D. melanogaster feeding assay. In conditions of low magnesium, the relA gene enhanced production of the cell-cell signal N-[3-oxododecanoyl]-l-homoserine lactone, whereas relA reduced the production of the 2-heptyl-3-hydroxy-4-quinolone signal during serine hydroxamate induction of the stringent response. In the relA mutant, alterations in the Pseudomonas quinolone system pathways seemed to increase the production of pyocyanin and decrease the production of elastase. Deletion of relA also resulted in reduced levels of the RpoS sigma factor. These results suggest that adjustment of cellular ppGpp and pppGpp levels could be an important regulatory mechanism in P. aeruginosa adaptation in pathogenic relationships.

Indexed as

Amino AcidsAnimalsBacterial ProteinsCystic FibrosisDrosophila melanogasterGuanosine PentaphosphateGuanosine TetraphosphateMutationPancreatic ElastasePseudomonas aeruginosaPyocyanineSerineSigma FactorVirulenceAmino AcidsBacterial ProteinsGuanosine PentaphosphateGuanosine TetraphosphatePancreatic ElastasePyocyanineSerineserine hydroxamateSigma Factorsigma factor KatF protein, Bacteria

Identifiers

PMID15385461
PMCPMC517598
OpenAlexW2164838577

What OpenQuestion holds

Textmetadata
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.