Natural C. elegans isolates feed on bacteria either alone or in groups1. Previous data has shown that social feeding is induced, at least in part, by signals from the nociceptive neurons ASH and ADL2. Apart from ASH and ADL, other neurons mediate avoidance behaviours in C. elegans, including the AWB neurons, which sense some repulsive odors. To ask whether AWB regulates aggregation behaviour, we genetically ablated this neuron in social
npr-1 animals using a
lim-4 mutation.
lim-4 is a LIM homeobox gene required for correct specification of AWB3.
lim-4 npr-1 mutant animals showed very weak social behaviour compared to
npr-1 mutants, suggesting that AWB upregulates social feeding. To investigate the potential role of AWB in social behaviour further, we analysed mutants defective in 2-nonanone avoidance. Avoidance of 2-nonanone is mediated by AWB, and is disrupted in animals lacking the transmembrane guanylyl cyclase DAF-114 and the cGMP-gated ion channel TAX-2/TAX-45. Mutations in both
daf-11 and
tax-4 abolish social feeding of
npr-1 animals. Using heterologous promoters, we dissected where DAF-11 and TAX-4 are required for social feeding. Our data suggest that both these genes are required in AWB neurons for social feeding behaviour. In a separate project, I have characterised new suppressors of social feeding behaviour. Two screens that were previously carried out identified about 50 mutations that convert
npr-1(null) social feeders into solitary feeders (see abstract by Cheung and de Bono). In an attempt to reach saturation, we carried out a third screen that identified a further 100 mutations that disrupt aggregation of
npr-1 animals. I mapped 7 of these suppressors to less than 600 kb. All these suppressors mate, dye-fill normally, and move well. One suppressor, represented by the allele
db44, failed to complement
tax-6, which encodes the C. elegans calcineurin A subunit6. The remaining 6 suppressors appear to define previously uncharacterised genes. I have cloned one of these,
db47, and shown it is mutated in the C. elegans homologue of Drosophila retinal degeneration B protein. 1 de Bono and Bargmann, 1998, Cell, 94:679-89; 2 de Bono et al., 2002, Nature 419:899-903; 3 Sagasti et al., 1999, Gene & Development, 13:1794-1806; 4 Birnby et al., 2000, Genetics 155:85-104; 5 Troemel et al., 1997, Cell 91:161-169; 6 Kuhara et al., 2002, Neuron, 33:751-763.