Many wild strains of C. elegans clump together on bacteria (R. Cassada, wm87 p162). A notable non-clumper is N2: N2 worms are solitary when well fed. We are examining how clumping is mediated in clumper strains and inhibited in N2. We have characterised the phenotypes of 4 non-complementing alleles which cause clumping, including 3 alleles isolated from mutagenised N2 (Davis and Avery, WBG 11.5p69; H.A. Colbert, pers. com), and an allele isolated from the wild strain RC301 (R. Cassada, ibid.). These mutations define the gene bor-1X. All four alleles are recessive and show the same set of phenotypes: clumping, bordering and burrowing. Unlike N2, bor-1 mutants also fail to slow down appreciably in response to bacteria, even after starvation, which sensitizes the N2 bacterial response. Homozygous and hemizygous mutants of at least two bor-1 alleles are indistinguishable, suggesting that they are loss-of-function mutations. We mapped bor-1 to a small region of X close to lon-2, and obtained rescue with a 24kb clone containing two predicted ORFs. We are currently narrowing the rescuing region further. Double mutants of bor-1 with mutations that disrupt chemosensory and mechanosensory behaviours clump as effectively as bor-1 single mutants, suggesting that clumping may define a new sensory modality. To study this behaviour we constructed double mutants of bor-1 with mutations that abolish various aspects of neuronal activity in the worm. So far only mutations in tax-2, tax-4, osm-9 and snt-1 suppress clumping. These genes may provide insight into the signal transduction pathway that mediates clumping. tax-2 and tax-4 encode subunits of a cyclic nucleotide gated ion channel and appear to be expressed in only 11 neurons. All bor-1 phenotypes are suppressed by tax-2 and tax-4 mutations, suggesting that these behaviours are coordinately regulated by one or a small number of neurons. In addition, the locomotory response of bor-1; tax-4 animals to bacteria is similar to that of N2 in both well fed and starved animals. This indicates that bor-1 activity per se is not required for response to bacteria, but rather that locomotion in bor-1 mutants is set at too high a level to be inhibited by food.

Affiliation:
- HHMI, Department of Anatomy, UCSF, Parnassus Avenue, San Francisco CA 94143, USA.