We are interested to study synaptic transmission by focusing on
unc-31 in C. elegans . Several lines of evidence suggest that
unc-31 plays a role in synaptic transmission. Firstly,
unc-31 animals are defective in a variety of behaviors including locomotion, egg-laying, pharyngeal pumping and dauer recovery. Secondly,
unc-31 is expressed in a variety of neurons. Thirdly, UNC-31 protein is the C. elegans homolog of mammalian CAPS (Calcium-dependent Activator Protein for Secretion): in PC12 cells, CAPS is necessary for DCV (Dense Core Vesicles) exocytosis but not for SV (Synaptic Vesicle or Small Clear Vesicles) exocytosis. DCVs contain catecholamins, neuropeptides or hormones, whereas SVs contain classical small neurotransmitters such as acetylcholin . These observations suggest that
unc-31 may play a role in DCV exocytosis. To elucidate the possible mechanism of
unc-31 action we are using both molecular and genetic approaches to identify molecules that potentially interact with UNC-31 or function in the same pathway. Using chemical mutagenesis we isolated 45 revertants of the
unc-31(
e928) mutant; all revertants can reverse the lethargic locomotory phenotype of
unc-31 mutants. Some revertants are hyperactive while others resemble the wild type locomotory phenotype. Using the yeast two-hybrid system we isolated a novel gene (C18B2.5) from a C. elegans cDNA library using
unc-31 cDNA as bait. Presently, we are characterizing the
unc-31 revertants and this novel gene.