Evidence map›Paper›PMID 21423671›Full record

ArticlePLoS pathogens2011

The moving junction protein RON8 facilitates firm attachment and host cell invasion in Toxoplasma gondii.

Kurtis W Straub, Eric D Peng, Bettina E Hajagos, Jessica S Tyler, Peter J Bradley

Abstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. TheBiology open · 2019
    Article
  11. How does Toxoplama gondii invade host cells?The Journal of veterinary medical science · 2018
    Review
  12. Article
  13. RON4Scientific reports · 2017
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Lytic Cycle of Toxoplasma gondii: 15 Years Later.Annual review of microbiology · 2015
    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

5 authors.

Kurtis W StraubDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA.
Eric D Peng
Bettina E Hajagos
Jessica S Tyler
Peter J Bradley

Funding

UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
Toxoplasma Rhoptry FunctionR01AI021423 · NIAID · STANFORD UNIVERSITY · PI BOOTHROYD, JOHN C · 1985 to 2018
$7.8M
The Role of Toxoplasma Rhoptries in Host Cell InfectionR01AI064616 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRADLEY, PETER JOHN · 2006 to 2016
$3.5M
ANTIGENS OF TOXOPLASMA GONDII AND THEIR GENESR37AI021423 · NIAID · STANFORD UNIVERSITY · PI BOOTHROYD, JOHN C · 1994 to 2003
$1.6M
NIAID NIH HHS R01 AI021423NIAID NIH HHS R01 AI064616NIAID NIH HHS R37 AI021423NIAID NIH HHS T32 AI007323NIAID NIH HHS T32-AI07323NIGMS NIH HHS GM07185NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

The apicomplexan moving junction (MJ) is a highly conserved structure formed during host cell entry that anchors the invading parasite to the host cell and serves as a molecular sieve of host membrane proteins that protects the parasitophorous vacuole from host lysosomal destruction. While recent work in Toxoplasma and Plasmodium has reinforced the composition of the MJ as an important association of rhoptry neck proteins (RONs) with micronemal AMA1, little is known of the precise role of RONs in the junction or how they are targeted to the neck subcompartment. We report the first functional analysis of a MJ/RON protein by disrupting RON8 in T. gondii. Parasites lacking RON8 are severely impaired in both attachment and invasion, indicating that RON8 enables the parasite to establish a firm clasp on the host cell and commit to invasion. The remaining junction components frequently drag in trails behind invading knockout parasites and illustrate a malformed complex without RON8. Complementation of Δron8 parasites restores invasion and reveals a processing event at the RON8 C-terminus. Replacement of an N-terminal region of RON8 with a mCherry reporter separates regions within RON8 that are necessary for rhoptry targeting and complex formation from those required for function during invasion. Finally, the invasion defects in Δron8 parasites seen in vitro translate to radically impaired virulence in infected mice, promoting a model in which RON8 has a crucial and unprecedented task in committing Toxoplasma to host cell entry.

Indexed as

AnimalsAntigens, ProtozoanCells, CulturedDisease Models, AnimalGene Knockout TechniquesHost-Parasite InteractionsHumansLongevityMembrane ProteinsMiceProtozoan ProteinsReceptor Protein-Tyrosine KinasesToxoplasmaToxoplasmosisAMA1 protein, Toxoplasma gondiiAntigens, ProtozoanMembrane ProteinsProtozoan ProteinsReceptor Protein-Tyrosine KinasesRON protein

Identifiers

PMID21423671
PMCPMC3053350

What OpenQuestion holds

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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.