Evidence map›Paper›PMID 24843160›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

The small GTPase RAB-11 directs polarized exocytosis of the intracellular pathogen N. parisii for fecal-oral transmission from C. elegans.

Suzannah C Szumowski, Michael R Botts, John J Popovich, Margery G Smelkinson, Emily R Troemel

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  13. Innate immunity in C. elegans.Current topics in developmental biology · 2021
    Review
  14. Article
  15. Article
  16. Invasion of Host Cells by Microsporidia.Frontiers in microbiology · 2020
    Review
  17. Article
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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.

Suzannah C SzumowskiDivision of Biological Sciences, Section of Cell and Developmental Biology, University of California at San Diego, La Jolla, CA 92093.
Michael R BottsDivision of Biological Sciences, Section of Cell and Developmental Biology, University of California at San Diego, La Jolla, CA 92093.
John J PopovichDivision of Biological Sciences, Section of Cell and Developmental Biology, University of California at San Diego, La Jolla, CA 92093.
Margery G SmelkinsonDivision of Biological Sciences, Section of Cell and Developmental Biology, University of California at San Diego, La Jolla, CA 92093.
Emily R TroemelDivision of Biological Sciences, Section of Cell and Developmental Biology, University of California at San Diego, La Jolla, CA 92093 etroemel@ucsd.edu.
University of California, San Diego · US

Funding

Training Program in Basic Clinical GeneticsT32GM008666 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMILTON, BRUCE A · 1998 to 2021
$8.6M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
A natural host model for microsporidia pathogenesis in the intestineR01AI087528 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TROEMEL, EMILY R · 2010 to 2014
$1.9M
NIAID NIH HHS R01 AI087528NIGMS NIH HHS T32 GM008666NIH HHS P40 OD010440
6 · The paper itself

Abstract

Pathogen exit is a key stage in the spread and propagation of infectious disease, with the fecal-oral route being a common mode of disease transmission. However, it is poorly understood which molecular pathways provide the major modes for intracellular pathogen exit and fecal-oral transmission in vivo. Here, we use the transparent nematode Caenorhabditis elegans to investigate intestinal cell exit and fecal-oral transmission by the natural intracellular pathogen Nematocida parisii, which is a recently identified species of microsporidia. We show that N. parisii exits from polarized host intestinal cells by co-opting the host vesicle trafficking system and escaping into the lumen. Using a genetic screen, we identified components of the host endocytic recycling pathway that are required for N. parisii spore exit via exocytosis. In particular, we show that the small GTPase RAB-11 localizes to apical spores, is required for spore-containing compartments to fuse with the apical plasma membrane, and is required for spore exit. In addition, we find that RAB-11-deficient animals exhibit impaired contagiousness, supporting an in vivo role for this host trafficking factor in microsporidia disease transmission. Altogether, these findings provide an in vivo example of the major mode of exit used by a natural pathogen for disease spread via fecal-oral transmission.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell CompartmentationCell MembraneCell PolarityExocytosisGastrointestinal TractHumansMembrane FusionMicroscopy, Electron, TransmissionMicrosporidiaSpores, FungalVesicular Transport ProteinsCaenorhabditis elegans Proteinsrab-11.1 protein, C elegansVesicular Transport Proteins

Identifiers

PMID24843160
PMCPMC4050618
OpenAlexW2038302914

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.