2004 West Coast Worm Meeting abstract 107

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Polyunsaturated Fatty Acids Modulate TRPV-dependent Chemosensory Signaling in vivo

Amanda Kahn-Kirby1,2, Jennifer Watts2,3, Jami L.M. Dantzker1, John Browse3, Cornelia I. Bargmann1

1 HHMI and University of California, San Francisco
2 These authors contributed equally
3 Washington State University, Pullman

The C. elegans osm-9 and ocr-2genes encode predicted cation channels that are essential for proper signal transduction in a subset of chemosensory neurons. osm-9 and ocr-2 are members of the conserved TRP ion channel family; they are most closely related to the mammalian capsaicin receptor TRPV1 and the osmolarity-sensing channel TRPV4. Several mechanisms have been proposed for the intracellular modulation of TRP channels, including facilitation or inhibition by a panoply of lipid molecules.  To date, genetic evidence for these models has been relatively scarce.  Our in vivogenetic analysis of C. elegansmutants in polyunsaturated fatty acid (PUFA) synthesis pathways suggests a role for specific PUFAs in osm-9 and ocr-2 signal transduction.

            C. elegans mutants in PUFA synthesis pathways were isolated by a gas chromatography-based screen, as previously described (Watts and Browse 2002).  Behavioral analysis established that a subset of mutants deficient in PUFA synthesis were strongly and specifically defective for chemosensory behaviors mediated by osm-9/ocr-2 signaling pathways, notably olfactory signaling in AWA neurons and avoidance signaling in ASH nociceptive neurons.  Dietary supplementation with PUFAs resulted in acute rescue of behavioral defects.  Direct exposure of animals to exogenous PUFAs resulted in a robust, TRPV-dependent avoidance behavior mediated by ASH, and in TRPV-dependent Ca2+ transients in the ASH nociceptive neurons.

            Our behavioral data demonstrates that specific PUFAs contribute to chemosensory neuron function in C. elegans.  We suggest that derivatives of these lipids are mobilized in sensory cilia by G-protein signaling pathways to modulate channel activity.

 

 

Watts and Browse, PNAS 99 (2002): 5854-5859.