4.8 Article

The G protein-coupled receptor FSHR-1 is required for the Caenorhabditis elegans innate immune response

Publisher

NATL ACAD SCIENCES
DOI: 10.1073/pnas.0813048106

Keywords

host-pathogen interactions; leucine-rich repeat

Funding

  1. National Institutes of Health (NIH) National Center for Research Resources
  2. NIH [P01 AI044220, R01 AI064332]
  3. Burroughs Wellcome Fund
  4. NIH National Institute of Allergy and Infectious Dieases K08 award
  5. Kirschstein National Research Service Award [F32 AI068376]

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Innate immunity is an ancient defense system used by both vertebrates and invertebrates. Previously characterized innate immune responses in plants and animals are triggered by detection of pathogens using specific receptors, which typically use a leucine-rich repeat (LRR) domain to bind molecular patterns associated with infection. The nematode Caenorhabditis elegans uses defense pathways conserved with vertebrates; however, the mechanism by which C. elegans detects pathogens is unknown. We screened all LRR-containing transmembrane receptors in C. elegans and identified the G protein-coupled receptor FSHR-1 as an important component of the C. elegans immune response to Gram-negative and Gram-positive bacterial pathogens. FSHR-1 acts in the C. elegans intestine, the primary site of exposure to ingested pathogens. FSHR-1 signals in parallel to the known p38 MAPK pathway but converges to regulate the transcriptional induction of an overlapping but nonidentical set of antimicrobial effectors. FSHR-1 may act generally to boost the nematode immune response, or it may function as a pathogen receptor.

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