The role of mycelium production and a MAPK-mediated immune response in the C. elegans-Fusarium model system

Maged Muhammed, Beth Burgwyn Fuchs, Michael P. Wu, Julia Breger, Jeffrey J. Coleman, Eleftherios Mylonakis

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


Fusariosis is an emerging infectious complication of immune deficiency, but models to study this infection are lacking. The use of the soil nematode Caenorhabditis elegans as a model host to study the pathogenesis of Fusarium spp. was investigated. We observed that Fusarium conidia consumed by C. elegans can cause a lethal infection and result in more than 90% killing of the host within 120 hours, and the nematode had a significantly longer survival when challenged with Fusarium proliferatum compared to other species. Interestingly, mycelium production appears to be a major contributor in nematode killing in this model system, and C. elegans mutant strains with the immune response genes, tir-1 (encoding a protein containing a TIR domain that functions upstream of PMK-1) and pmk-1 (the homolog of the mammalian p38 MAPK) lived significantly shorter when challenged with Fusarium compared to the wild type strain. Furthermore, we used the C. elegans model to assess the efficacy and toxicity of various compounds against Fusarium. We demonstrated that amphotericin B, voriconazole, mancozeb, and phenyl mercury acetate significantly prolonged the survival of Fusarium-infected C. elegans, although mancozeb was toxic at higher concentrations. In conclusion, we describe a new model system for the study of Fusarium pathogenesis and evolutionarily preserved host responses to this important fungal pathogen.

Original languageEnglish (US)
Pages (from-to)488-496
Number of pages9
JournalMedical Mycology
Issue number5
StatePublished - Jul 2012


  • Caenorhabditis elegans
  • Fusarium
  • Host
  • Mancozeb

ASJC Scopus subject areas

  • Infectious Diseases


Dive into the research topics of 'The role of mycelium production and a MAPK-mediated immune response in the C. elegans-Fusarium model system'. Together they form a unique fingerprint.

Cite this