Worm Breeder's Gazette 13(5): 86 (February 1, 1995)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Expression of osm-3 Kinesin Gene Is Exclusively Limited To a Set of 26 Chemosensory Neurons in C. elegans That Are Open To The External Environment.

M. Tabish1, Z. K. Siddiqui1, K. Nishikawa2, S. S. Siddiqui1

1 Laboraotry of Molecular Biology, Toyohashi University of Technology, Japan 441.
2 Protein Engineering Research Institute, Osaka 565, Japan

Previously three genetic loci osm-3, unc-104, and unc-116
have been described in C. elegans which encode anterograde
motor kinesin proteins 3. We have now determined the complete
structure of the osm-3 gene which encodes a kinesin like
protein of 672 amino acids. OSM-3 consists of all three
functional domains generally found in kinesin heavy chain
proteins, including an amino terminal globular motor
region containing an ATP binding site, an alpha helical
coiled coil rod region, and a globular tail domain located
at the carboxyl terminus. The OSM-3 kinesin shows homology
in both the motor and rod domains with kinesins from divergent
species such as mouse KIF3, and sea urchin KRP95, and also
with the rod domains of several non kinesin proteins, such
as myosin, ezrin, outer membrane alpha precursor OMPA,
yeast intracellular protein transport USO1, and the rat
neurofilament NF-H. Temporal and spatial expression
pattern of the osm-3 gene was determined by using the 1.9
kb osm- 3 promoter region from a 4.5 kb genomic fragment
that can rescue the osm-3 mutant phenotype in germline
transgenic animals. An osm-3::lacZ fusion gene was constructed
in the pPD22.11 expression vector (A. Fire), which included
the nuclear localization signal. Histochemical staining
of transformants revealed that the fusion gene expression
is limited to an exclusive set of 26 chemosensory neurons
whose dendritic endings are open to the outside environment
through a hole in the animal's cuticle. These include six
IL2 neurons of the inner labial sensilla, eight pairs of
amphid neurons (ADF, ADL, ASE, ASG, ASH, ASI, ASJ, and ASK)
in the head, and two pairs of phasmid neurons (PHA, and PHB)
in lumbar ganglia in the tail. Ultrastructurally the osm-3(P802)
mutant has a shortening of the distal tip of the amphid neurons,
but a normal structure of the IL2 neurons. An even more intriguing
observation concerns with the temporal expression of
the fusion gene, as staining of IL2 and amphid and phasmid
neurons can be seen in early larval stages (L1-L2); however,
in late larval and adult stages the staining of amphid neurons
completely disappears, but continues in the IL2 and phasmid
neurons with the same intensity as observed in early larval
stages, suggesting that the osm-3 gene is differentially
expressed in all three different chemosensory sensilla.
We are now interested in examining the normal and ectopic
expression of the osm-3 gene in a variety of mutants altered
in sensory and other behaviors. We thank A. Coulson, A.
Fire, R., Horvitz, J. Miwa, T. Sano, for help in this work.
(References: 1: Shakir et al., 1993; 2: Otsuka et al., 1991,
Hall and Hedgecock, 1991; 3: Patel et al., 1993; 4: Perkins
et al. 1986)