Evidence map›Paper›PMID 17071752›Full record

ArticleJournal of bacteriology2007

Mutations in the Yersinia pseudotuberculosis type III secretion system needle protein, YscF, that specifically abrogate effector translocation into host cells.

Alison J Davis, Joan Mecsas

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Cryo-EM structure of the needle filament tip complex of theProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. TheMicroorganisms · 2021
    Review
  7. Article
  8. The type III secretion system needle, tip, and translocon.Protein science : a publication of the Protein Society · 2019
    Review
  9. Article
  10. Article
  11. Life After Secretion-Frontiers in microbiology · 2019
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. The type III secretion system apparatus determines the intracellular niche of bacterial pathogens.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Alison J DavisDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA.
Joan Mecsas
Tufts University · US

Funding

Yersinia Yops in an Animal Infection ModelR01AI056068 · NIAID · TUFTS UNIVERSITY BOSTON · PI MECSAS, JOAN C. · 2003 to 2007
$1.8M
Inhibitors of Yersinia Yop Type III Secretion(RMI)R21NS053740 · NINDS · TUFTS UNIVERSITY BOSTON · PI MECSAS, JOAN C. · 2005 to 2005
$181k
Identification of Xcv TTSS componentsF32GM067517 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI DAVIS, ALISON J · 2003 to 2005
$147k
NIAID NIH HHS R01 AI056068NIGMS NIH HHS F32 GM067517NIGMS NIH HHS GM67517NINDS NIH HHS R21 NS053740PHS HHS P3034928
6 · The paper itself

Abstract

The trafficking of effectors, termed Yops, from Yersinia spp. into host cells is a multistep process that requires the type III secretion system (TTSS). The TTSS has three main structural parts: a base, a needle, and a translocon, which work together to ensure the polarized movement of Yops directly from the bacterial cytosol into the host cell cytosol. To understand the interactions that take place at the interface between the tip of the TTSS needle and the translocon, we developed a screen to identify mutations in the needle protein YscF that separated its function in secretion from its role in translocation. We identified 25 translocation-defective (TD) yscF mutants, which fall into five phenotypic classes. Some classes exhibit aberrant needle structure and/or reduced levels of Yop secretion, consistent with known functions for YscF. Strikingly, two yscF TD classes formed needles and secreted Yops normally but displayed distinct translocation defects. Class I yscF TD mutants showed diminished pore formation, suggesting incomplete pore insertion and/or assembly. Class II yscF TD mutants formed pores but showed nonpolar translocation, suggesting unstable needle-translocon interactions. These results indicate that YscF functions in Yop secretion and translocation can be genetically separated. Furthermore, the identification of YscF residues that are required for the assembly of the translocon and/or productive interactions with the translocon has allowed us to initiate the mapping of the needle-translocon interface.

Indexed as

Bacterial ProteinsBiological TransportCell Line, TumorHumansMembrane ProteinsModels, MolecularMutationYersinia pseudotuberculosisYersinia pseudotuberculosis InfectionsBacterial ProteinsMembrane Proteins

Identifiers

PMID17071752
PMCPMC1797200
OpenAlexW2162082832

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.