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Nature 419, 899-903 (31 October 2002) | doi:10.1038/nature01169; Received 24 June 2002; Accepted 30 September 2002

Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli

Mario de Bono1,2, David M. Tobin1, M. Wayne Davis3,4, Leon Avery3 & Cornelia I. Bargmann1

  1. Howard Hughes Medical Institute, Programs in Developmental Biology, Neuroscience, and Genetics, Departments of Anatomy and Biochemistry & Biophysics, UCSF, California 94143-0452, USA
  2. MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK
  3. Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, Texas 75390-9148, USA
  4. Present address: Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, Utah 84112-0840, USA.

Correspondence to: Mario de Bono1,2 Correspondence and requests for materials should be addressed to M.d.B. (e-mail: Email: debono@mrc-lmb.cam.ac.uk).

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Natural Caenorhabditis elegans isolates exhibit either social or solitary feeding on bacteria. We show here that social feeding is induced by nociceptive neurons that detect adverse or stressful conditions. Ablation of the nociceptive neurons ASH and ADL transforms social animals into solitary feeders. Social feeding is probably due to the sensation of noxious chemicals by ASH and ADL neurons; it requires the genes ocr-2 and osm-9, which encode TRP-related transduction channels, and odr-4 and odr-8, which are required to localize sensory chemoreceptors to cilia. Other sensory neurons may suppress social feeding, as social feeding in ocr-2 and odr-4 mutants is restored by mutations in osm-3, a gene required for the development of 26 ciliated sensory neurons. Our data suggest a model for regulation of social feeding by opposing sensory inputs: aversive inputs to nociceptive neurons promote social feeding, whereas antagonistic inputs from neurons that express osm-3 inhibit aggregation.