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

**Authors:** Han-Wen Chang, Hung-Che Lin, Ching-Ting Yang, Rebecca J. Tay, Dao-Ming Chang, Yi-Chung Tung, Yen-Ping Hsueh, Roland Roberts, Roland Roberts, Roland Roberts

PMC · DOI: 10.1371/journal.pbio.3003178 · PLOS Biology · 2025-07-01

## TL;DR

Nematodes can avoid being trapped by fungi by altering their cuticle, but this makes them more fragile and sensitive to stress.

## Contribution

The study identifies a nuclear hormone receptor that regulates nematode cuticle structure to evade fungal predation.

## Key findings

- Loss-of-function mutations in NHR-66 reduce nematode adhesion to fungal traps.
- Cuticular collagens are essential for fungal-nematode adhesion.
- NHR-66 mutants show increased sensitivity to hypoosmotic stress and cuticular fragility.

## 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.

How do nematodes avoid fungal predators? This study reveals that a nuclear hormone receptor alters the nematode cuticle, allowing them to evade fungal adhesive traps. This comes at a cost, however, as the escaping nematodes are more delicate and sensitive to osmotic stress.

## Linked entities

- **Genes:** nhr-66 (Nuclear hormone receptor family member nhr-66) [NCBI Gene 177618]
- **Species:** Caenorhabditis elegans (taxon 6239)

## Full-text entities

- **Genes:** col-64 (Nematode cuticle collagen N-terminal domain-containing protein) [NCBI Gene 186127], nhr-66 (Nuclear hormone receptor family member nhr-66) [NCBI Gene 177618]
- **Diseases:** fungal (MESH:D009181), hypersensitivity (MESH:D004342)
- **Species:** Caenorhabditis elegans (species) [taxon 6239], Arthrobotrys oligospora [taxon 13349], Nematoda (nematode, phylum) [taxon 6231], C. elegans [taxon 328850]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12237271/full.md

## References

49 references — full list in the complete paper: https://tomesphere.com/paper/PMC12237271/full.md

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Source: https://tomesphere.com/paper/PMC12237271