C. elegans is predicted to express approximately 250 neuropeptides. Many of these have potent biological activity. A subset of more than forty G-protein-coupled receptors (GPCR) are candidates for mediating these effects. As part of a long-term goal to pair neuropeptide receptors with their cognate ligands, we have been carrying out a systematic analysis of GPCR gene deletion mutants. Gene deletion mutants have been supplied by the C. elegans knockout consortia for C10C6.2 (
npr-3), C16D6.2, C25G6.5, C39E6.6 (
npr-1), C53C7.1, C56G3.1, F35G8.1, F41E7.3, T05A1.1 (
npr-2), T22D1.12, Y58G8A.4, ZC412.1, C30F12.6, C38C10.1, C43C3.2, C48C5.1, F57H12.4, Y54E2A.1, ZK455.3. The deletions have been sequenced and the strains out-crossed four or more times. As neuropeptides have been shown to have potent effects on the body wall and pharyngeal muscle of nematodes, we have assayed these mutants for defects in thrashing and pharyngeal pumping on food. Animals which have defects in thrashing have been further tested for aldicarb sensitivity in order to determine whether there is altered cholinergic signalling at the neuromuscular junction. Mutants with altered pharyngeal pumping were further analysed using electropharyngeogram recordings. These mutants were also tested for altered responses to neuropeptides which have previously been shown to have potent effects in this preparation. The majority of the GPCR mutants do not show any overt phenotype. The thrashing assay has identified two mutants with defects in this behaviour,
npr-2 (
ok419), and a deletion in C10C6.2,
npr-3 (
tm1583). So far, none of the mutants exhibit altered pharyngeal pumping behaviour. Funded by the BBSRC, UK. Thanks to the C. elegans knockout consortia (NBRP Japan and USA) for the provision of strains.