Evidence map›Paper›PMID 9746567›Full record

ArticleInfection and immunity1998

Identification of two Shigella flexneri chromosomal loci involved in intercellular spreading.

M Hong, Y Gleason, E E Wyckoff, S M Payne

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Hypothetical Proteins ofMicroorganisms · 2023
    Article
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  7. Complexity of Complement Resistance Factors Expressed byJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  8. Article
  9. How Do the Virulence Factors ofFrontiers in cellular and infection microbiology · 2017
    Review
  10. Article
  11. Molecular and Cellular Mechanisms of Shigella flexneri Dissemination.Frontiers in cellular and infection microbiology · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. An ABC transport system that maintains lipid asymmetry in the gram-negative outer membrane.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

4 authors at 1 institution in 1 country.

M HongDepartment of Microbiology and Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas 78712, USA.
Y Gleason
E E Wyckoff
S M Payne
The University of Texas at Austin · US

Funding

ROLE OF CARBON METABOLISM AND VIRULENCE OF SHIGELLA FLEXNERIR37AI016935 · NIAID · UNIVERSITY OF TEXAS AUSTIN · PI Shelley M. Payne · 2003 to 2026
$6.0M
Role of carbon metabolism in virulence of Shigella flexneriR01AI016935 · NIAID · UNIVERSITY OF TEXAS AUSTIN · PI PAYNE, SHELLEY M. · 1985 to 2017
$2.6M
NIAID NIH HHS AI 16935NIAID NIH HHS R01 AI016935NIAID NIH HHS R37 AI016935
6 · The paper itself

Abstract

The ability of Shigella flexneri to multiply within colonic epithelial cells and spread to adjacent cells is essential for production of dysentery. Two S. flexneri chromosomal loci that are required for these processes were identified by screening a pool of TnphoA insertion mutants. These mutants were able to invade cultured epithelial cells but could not form wild-type plaques. Analysis of the nucleotide sequence indicated that the sites of TnphoA insertion were within two different regions that are almost identical to Escherichia coli K-12 chromosomal sequences of unknown functions. One region is located at 70 min on the E. coli chromosome, upstream of murZ, while the other is at 28 min, downstream of tonB. The mutant with the insertion at 70 min was named vpsC because it showed an altered pattern of virulence protein secretion. The vpsC mutant formed pinpoint-sized plaques, was defective in recovery from infected tissue culture cells, and was sensitive to lysis by the detergent sodium dodecyl sulfate. Recombinant plasmids carrying the S. flexneri vpsA, -B, and -C genes complemented all of the phenotypes of the vpsC mutant. A mutation in vpsA resulted in the same phenotype as the vpsC mutation, suggesting that these two genes are part of a virulence operon in S. flexneri. The mutant with the insertion at 28 min was interrupted in the same open reading frame as S. flexneri ispA. This ispA mutant could not form plaques and was defective in bacterial septation inside tissue culture cells.

Indexed as

Genes, BacterialMembrane ProteinsBacterial ProteinsCell Membrane PermeabilityCells, CulturedChromosomes, BacterialCloning, MolecularCongo RedDeoxycholic AcidGenetic Complementation TestHeminLoop of HenleMolecular Sequence DataMutagenesis, InsertionalOperonPhenotypeBacterial ProteinsCongo RedDeoxycholic AcidHeminIspA protein, Shigella flexneriMembrane ProteinsSodium Dodecyl SulfateVpsA protein, Shigella flexneriVpsB protein, Shigella flexneriVpsC protein, Shigella flexneri

Identifiers

PMID9746567
PMCPMC108578
OpenAlexW2141848152

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.