iScience (Apr 2024)

Caenorhabditis elegans neuropeptide NLP-27 enhances neurodegeneration and paralysis in an opioid-like manner during fungal infection

  • Maria Pop,
  • Anna-Lena Klemke,
  • Lena Seidler,
  • Nicole Wernet,
  • Pietrina Loredana Steudel,
  • Vanessa Baust,
  • Elke Wohlmann,
  • Reinhard Fischer

Journal volume & issue
Vol. 27, no. 4
p. 109484

Abstract

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Summary: The nervous system of metazoans is involved in host-pathogen interactions to control immune activation. In Caenorhabditis elegans, this includes sleep induction, mediated by neuropeptide-like proteins (NLPs), which increases the chance of survival after wounding. Here we analyzed the role of NLP-27 in the infection of C. elegans with the nematode-trapping fungus Arthrobotrys flagrans. Early responses of C. elegans were the upregulation of nlp-27, the induction of paralysis (sleep), and neurodegeneration of the mechanosensing PVD (Posterior Ventral Process D) neurons. Deletion of nlp-27 reduced neurodegeneration during fungal attack. Induction of nlp-27 was independent of the MAP kinase PMK-1, and expression of nlp-27 in the hypodermis was sufficient to induce paralysis, although NLP-27 was also upregulated in head neurons. NLP-27 contains the pentapeptide YGGYG sequence known to bind the human μ- and κ-type opioid receptors suggesting NLP-27 or peptides thereof act on opioid receptors. The opioid receptor antagonist naloxone shortened the paralysis time like overexpression of NLP-27.

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