Synaptic transmission is a highly regulated process that depends on the precise transport of organelles or vesicles via the micro tubule - based transport in the axonal transport and dendritic termini. Kinesins constitute micro tubule-based motor proteins and are essential for the axonal transport. The
osm-3 gene encodes a kinesin-like protein homolog of the heavy chain subunits of antergrade motor kinesin. The protein is required for formation of the distal segment of amphid channel cilia for responses to osmotic stimuli. During genetic screening of mutants defective in habituation induced by repetitive mechanical stimuli with C.elegans, we identified the
osm-3 gene allele,
cn350. We therefore tested behavior phenotype with available five
osm-3 alleles,
mn391,
hf3,
n1545,
n1540 and
p802.
cn350 and
mn391 animals were slowly habituated but rapidly recovered from habituation. We could not detect any visible abnormality on the habituation phenotype in the remaining four alleles. Wild-type animals show chemotaxis to NaCl, but avoid NaCl after conditioning with NaCl and starvation(1). The six
osm-3 alleles were abnormal on the plasticity of the salt chemotaxis: defectiveness in chemotactic ability
(hf3), maintenance of chemotactic ability after the conditioning
(mn391 and
cn350), and partial loss of chemotactic ability after the conditioning (
p802,
n1545 and
n1540).We are now determining mutation sites of the 6 alleles and detailed localization of OSM-3. OSM-3 functions as cargo that transports synaptic factors from cell bodies to synaptic terminals including synaptic vesicles. We therefore determing transport of OSM-3 in neural processes. (1) S.Saeki, M.Yamamoto and Y.Iino (2001). Plasticity of chemotaxis revealed by paired presentation of a chemoattractant and starvation in the nematode Caenorhabditis elegans. JEB204, 1757-1764