1. MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK
2. Present address: Department of Plant Sciences, University of Cambridge, Cambridge, UK.

Correspondence to: Mario de Bono¹ Correspondence and requests for materials should be addressed to M.d.B. (e-mail: Email: debono@mrc-lmb.cam.ac.uk).

Abstract

Wild isolates of Caenorhabditis elegans can feed either alone or in groups^{1, 2}. This natural variation in behaviour is associated with a single residue difference in NPR-1, a predicted G-protein-coupled neuropeptide receptor related to Neuropeptide Y receptors². Here we show that the NPR-1 isoform associated with solitary feeding acts in neurons exposed to the body fluid to inhibit social feeding. Furthermore, suppressing the activity of these neurons, called AQR, PQR and URX, using an activated K⁺ channel, inhibits social feeding. NPR-1 activity in AQR, PQR and URX neurons seems to suppress social feeding by antagonizing signalling through a cyclic GMP-gated ion channel encoded by tax-2 and tax-4. We show that mutations in tax-2 or tax-4 disrupt social feeding, and that tax-4 is required in several neurons for social feeding, including one or more of AQR, PQR and URX. The AQR, PQR and URX neurons are unusual in C. elegans because they are directly exposed to the pseudocoelomic body fluid³. Our data suggest a model in which these neurons integrate antagonistic signals to control the choice between social and solitary feeding behaviour.

1. MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK
2. Present address: Department of Plant Sciences, University of Cambridge, Cambridge, UK.

Correspondence to: Mario de Bono¹ Correspondence and requests for materials should be addressed to M.d.B. (e-mail: Email: debono@mrc-lmb.cam.ac.uk).