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The cysteine-rich virulence factor NipA of Arthrobotrys flagrans interferes with cuticle integrity of Caenorhabditis elegans

Summary

Researchers discovered how a predatory fungus attacks roundworms by producing a special protein called NipA that weakens the worm’s protective outer layer. This cysteine-rich protein causes blister-like formations in the worm’s skin and disrupts the genes responsible for maintaining the protective barrier. Understanding this mechanism helps scientists learn how fungi infect organisms and could lead to better control methods for parasitic nematodes.

Background

Nematode-trapping fungi like Arthrobotrys flagrans overcome the cuticle barrier of C. elegans to colonize the nematode body. While lytic enzymes are important for infection, small-secreted proteins (SSPs) without enzymatic activity have emerged as crucial virulence factors in fungal-nematode interactions.

Objective

To characterize NipA (nematode-induced protein A), a small-secreted cysteine-rich protein from A. flagrans, and determine its role in facilitating fungal penetration of C. elegans by interfering with cuticle integrity.

Results

NipA is a 133 amino acid cysteine-rich protein secreted at the fungal penetration site. Deletion of nipA delayed fungal penetration by ~13 minutes. Heterologous expression of NipA in nematode epidermis caused blister formation and altered expression of genes involved in extracellular matrix maintenance and innate immunity, particularly downregulating collagen genes like bli-6.

Conclusion

NipA is a virulence factor that facilitates fungal infection by disrupting cuticle integrity through interference with extracellular matrix components, allowing faster fungal penetration and colonization of C. elegans.
  • Published in:Nature Communications,
  • Study Type:Experimental Research,
  • Source: PMID: 38987250, DOI: 10.1038/s41467-024-50096-4
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