ArticleNature communications2024
The cysteine-rich virulence factor NipA of Arthrobotrys flagrans interferes with cuticle integrity of Caenorhabditis elegans.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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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.
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Who cites it
7 citing papers in PubMed.
- Virulensome: a transient organelle mediating fungal virulence.Science China. Life sciences · 2026Article
- Article
- WC1/WC2-Sre1 Transcriptional Cascade Controls Predation and Chlamydospore Formation in the Nematode-Trapping Fungus Arthrobotrys flagrans.Microbial biotechnology · 2026Article
- AoChk1 Is Required for Sporulation, Trap Formation, and Metabolic Process inJournal of fungi (Basel, Switzerland) · 2025Article
- FlbD: A Regulator of Hyphal Growth, Stress Resistance, Pathogenicity, and Chlamydospore Production in the Nematode-Trapping FungusMicroorganisms · 2025Article
- The Egh16-like virulence factor TrsA of the nematode-trapping fungus Arthrobotrys flagrans facilitates intrusion into its host Caenorhabditis elegans.PLoS pathogens · 2025Article
- Predation by nematode-trapping fungus triggers mechanosensory-dependent quiescence iniScience · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Animals protect themself from microbial attacks by robust skins or a cuticle as in Caenorhabditis elegans. Nematode-trapping fungi, like Arthrobotrys flagrans, overcome the cuticle barrier and colonize the nematode body. While lytic enzymes are important for infection, small-secreted proteins (SSPs) without enzymatic activity, emerge as crucial virulence factors. Here, we characterized NipA (nematode induced protein) which A. flagrans secretes at the penetration site. In the absence of NipA, A. flagrans required more time to penetrate C. elegans. Heterologous expression of the fungal protein in the epidermis of C. elegans led to blister formation. NipA contains 13 cysteines, 12 of which are likely to form disulfide bridges, and the remaining cysteine was crucial for blister formation. We hypothesize that NipA interferes with cuticle integrity to facilitate fungal entry. Genome-wide expression analyses of C. elegans expressing NipA revealed mis-regulation of genes associated with extracellular matrix (ECM) maintenance and innate immunity.
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Registered trials
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 Socratic graph.