Evidence map›Paper›PMID 23630961›Full record

ArticleInfection and immunity2013

A phenotype at last: essential role for the Yersinia enterocolitica Ysa type III secretion system in a Drosophila melanogaster S2 cell model.

Kimberly A Walker, Vivien I Maltez, Joshua D Hall, Nicholas P Vitko, Virginia L Miller

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Environmental Regulation of Yersinia Pathophysiology.Frontiers in cellular and infection microbiology · 2016
    Review
  13. Type III secretion systems: the bacterial flagellum and the injectisome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Kimberly A WalkerDepartment of Genetics, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA. kawalker@med.unc.edu
Vivien I Maltez
Joshua D Hall
Nicholas P Vitko
Virginia L Miller
University of North Carolina at Chapel Hill · US

Funding

SEEDING POSTDOCTORAL INNOVATORS IN RESEARCH &EDUCATIONK12GM000678 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DONALD T LYSLE, Kathryn Joanna Reissner · 1999 to 2026
$30.9M
YsrRS regulon of Y. enterocoliticaR01AI063299 · NIAID · WASHINGTON UNIVERSITY · PI MILLER, VIRGINIA L · 2005 to 2009
$1.1M
NIAID NIH HHS AI063299NIAID NIH HHS R01 AI063299NIGMS NIH HHS K12 GM000678NIGMS NIH HHS K12GM000678
6 · The paper itself

Abstract

The highly pathogenic Yersinia enterocolitica strains have a chromosomally encoded type III secretion system (T3SS) that is expressed and functional in vitro only when the bacteria are cultured at 26 °C. Mutations that render this system nonfunctional are slightly attenuated in the mouse model of infection only following an oral inoculation and only at early time points postinfection. The discrepancy between the temperature required for the Ysa gene expression and the physiological temperature required for mammalian model systems has made defining the role of this T3SS challenging. Therefore, we explored the use of Drosophila S2 cells as a model system for studying Ysa function. We show here that Y. enterocolitica is capable of infecting S2 cells and replicating intracellularly to high levels, an unusual feature of this pathogen. Importantly, we show that the Ysa T3SS is required for robust intracellular replication. A secretion-deficient mutant lacking the secretin gene, ysaC, is defective in replication within S2 cells, marking the first demonstration of a pronounced Ysa-dependent virulence phenotype. Establishment of S2 cells as a model for Y. enterocolitica infection provides a versatile tool to elucidate the role of the Ysa T3SS in the life cycle of this gastrointestinal pathogen.

Indexed as

Bacterial Secretion SystemsPhenotypeAnimalsBacterial LoadBacterial ProteinsCell LineCytoplasmDisease Models, AnimalDrosophila melanogasterGenes, BacterialGenetic Complementation TestMicroscopy, FluorescenceMutationPromoter Regions, GeneticProtein TransportTime FactorsBacterial ProteinsBacterial Secretion Systems

Identifiers

PMID23630961
PMCPMC3697602
OpenAlexW2089164907

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.