Evidence map›Paper›PMID 40591707›Full record

ArticlePLoS biology2025

Cuticular collagens mediate cross-kingdom predator-prey interactions between trapping fungi and nematodes.

Han-Wen Chang, Hung-Che Lin, Ching-Ting Yang, Rebecca J Tay, Dao-Ming Chang, Yi-Chung Tung, Yen-Ping Hsueh

Abstract read
In one paragraph

Article in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Han-Wen ChangMolecular and Cell Biology, Taiwan International Graduate Program, Academia Sinica and Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
Hung-Che LinInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Ching-Ting YangInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Rebecca J TayInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
Dao-Ming ChangResearch Center of Applied Sciences, Academia Sinica, Taipei, Taiwan.
Yi-Chung TungResearch Center of Applied Sciences, Academia Sinica, Taipei, Taiwan.
Yen-Ping HsuehMolecular and Cell Biology, Taiwan International Graduate Program, Academia Sinica and Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.ORCID 0000-0002-9052-5411

Funding

Academia Sinica Investigator AwardAcademia Sinica Postdoctoral FellowshipMax Planck Society
6 · The paper itself

Abstract

Adhesive interactions, mediated by specific molecular and structural mechanisms, are fundamental to host-pathogen and predator-prey relationships, driving evolutionary dynamics and ecological interactions. Here, we investigate the cellular and molecular basis of adhesion between the nematode Caenorhabditis elegans and its natural predator, the nematode-trapping fungus Arthrobotrys oligospora, which employs specialized adhesive nets to capture its prey. Using forward genetic screens, we identified C. elegans mutants that escape fungal traps and revealed the nuclear hormone receptor NHR-66 as a key regulator of fungal-nematode adhesion. Loss-of-function mutations in nhr-66 conferred resistance to fungal trapping through the downregulation of a large subset of cuticular collagen genes. Restoring collagen gene expression in nhr-66 mutants abolished the escape phenotype, highlighting the essential role of these structural proteins in fungal-nematode adhesion. Furthermore, sequence analysis of natural C. elegans populations revealed no obvious loss-of-function variants in nhr-66, suggesting selective pressures exist that balance adhesion-mediated predation risk with physiological robustness. We observed that loss of nhr-66 function resulted in a trade-off of increased hypersensitivity to hypoosmotic stress and cuticular fragility. These findings underscore the pivotal role of structural proteins in shaping ecological interactions and the evolutionary arms race between predator and prey.

Indexed as

AscomycotaCaenorhabditis elegansCollagenPredatory BehaviorAnimalsCaenorhabditis elegans ProteinsHost-Pathogen InteractionsMutationNematodaReceptors, Cytoplasmic and NuclearCaenorhabditis elegans ProteinsCollagenReceptors, Cytoplasmic and Nuclear

Identifiers

PMID40591707
PMCPMC12237271

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Registered trials

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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.