Evidence map›Paper›PMID 26057124›Full record

ArticlePloS one2015

Disruption of the C. elegans Intestinal Brush Border by the Fungal Lectin CCL2 Phenocopies Dietary Lectin Toxicity in Mammals.

Katrin Stutz, Andres Kaech, Markus Aebi, Markus Künzler, Michael O Hengartner

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. The interplay betweeniScience · 2025
    Article
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  7. Article
  8. Review
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  11. Review
  12. Article
  13. Journal of developmental biology · 2020
    Review
  14. Tepary bean (Toxicology research · 2020
    Article
  15. Article
  16. Article
  17. CNL-Molecules (Basel, Switzerland) · 2019
    Review
  18. Article
  19. The C. elegans model in toxicity testing.Journal of applied toxicology : JAT · 2017
    Review
  20. 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 2 institutions in 1 country.

Katrin StutzInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Andres KaechCenter for Microscopy and Image Analysis, University of Zurich, Zurich, Switzerland.
Markus AebiInstitute of Microbiology, ETH Zurich, Zurich, Switzerland.
Markus KünzlerInstitute of Microbiology, ETH Zurich, Zurich, Switzerland.
Michael O HengartnerInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
University of Zurich · CHETH Zurich · CH

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

Lectins are non-immunoglobulin carbohydrate-binding proteins without enzymatic activity towards the bound carbohydrates. Many lectins of e.g. plants or fungi have been suggested to act as toxins to defend the host against predators and parasites. We have previously shown that the Coprinopsis cinerea lectin 2 (CCL2), which binds to α1,3-fucosylated N-glycan cores, is toxic to Caenorhabditis elegans and results in developmental delay and premature death. In this study, we investigated the underlying toxicity phenotype at the cellular level by electron and confocal microscopy. We found that CCL2 directly binds to the intestinal apical surface and leads to a highly damaged brush border with loss of microvilli, actin filament depolymerization, and invaginations of the intestinal apical plasma membrane through gaps in the terminal web. We excluded several possible toxicity mechanisms such as internalization and pore-formation, suggesting that CCL2 acts directly on intestinal apical plasma membrane or glycocalyx proteins. A genetic screen for C. elegans mutants resistant to CCL2 generated over a dozen new alleles in bre 1, ger 1, and fut 1, three genes required for the synthesis of the sugar moiety recognized by CCL2. CCL2-induced intestinal brush border defects in C. elegans are similar to the damage observed previously in rats after feeding the dietary lectins wheat germ agglutinin or concanavalin A. The evolutionary conserved reaction of the brush border between mammals and nematodes might allow C. elegans to be exploited as model organism for the study of dietary lectin-induced intestinal pathology in mammals.

Indexed as

AllelesAnimalsCaenorhabditis elegansCell MembraneChemokine CCL2DietFungal ProteinsFungiGenetic TestingGlycocalyxIntestinal MucosaIntestinesLectinsMammalsChemokine CCL2Fungal ProteinsLectins

Identifiers

PMID26057124
PMCPMC4461262
OpenAlexW590071134

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.