Worm Breeder's Gazette 10(1): 85
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.
The mutant unc-104 (rh43) is paralyzed, and grows slowly. The epidermis is markedly reduced in volume along all four longitudinal cords. Cell lineages and axon trajectories that have been examined appear normal. The dorsal and ventral nerve cords are fully formed, the amphidial and phasmidial nerves appear normal, there is a nerve ring, and the PVP processes appear normal. Some muscle arms from the dorsal body muscles extend medially to the dorsal nerve cord in fairly normal fashion, but others extend ventrally towards the ventral muscles and possibly to the ventral nerve cord. Close examination of the dorsal and ventral nerve cords has revealed a complete absence of neuromuscular junctions (NMJs), despite the presence of motoneuron axons in the proper positions relative to the nerve/muscle plate. A normal NMJ consists of a vesicle-filled swelling of the presynaptic motor axon with an electron dense structure attached to the inside of the presynaptic membrane directly apposed to the postsynaptic muscle arms. In unc-104, the motor axons themselves seem deficient in synaptic vesicles along their length, although occasional clusters of vesicles are present. No presynaptic densities are seen associated with these clusters in motor axons in either motor nerve. The general lack of chemical synapses or NMJs within the nerve cords led us to examine the nerve ring in unc-104 in order to look for directed chemical synapses. Processes in the nerve ring are also deficient in synaptic vesicles, and no presynaptic densities are found in association with the relatively few axon swellings which do contain vesicles. It is possible that nondirected release of chemical transmitter(s) might still occur from these swellings, but the level of chemical synaptic transmission is presumably very low compared to wild type. Electrical transmission between neurons is probably still effective, since gap junctions between neurons are still found. The lack of presynaptic densities at neuron-neuron contacts within the nerve ring, as well as at neuron-muscle contacts along the motor nerves strongly suggests that unc-104 may be a gene product used to make these structures in the wild type. Another possibility is that the gene product is required more generally in the process of cell- cell recognition prior to forming a synapse. Many neuron cell bodies in the vicinity of the nerve ring appear to be filled with synaptic vesicles, as are occasional neuron cell bodies in the ventral cord. This is in contrast to the few vesicles within the axons, so one could argue that unc104 involves a defect in axonal transport. Alternately, vesicle transport down the axon may be reduced in the absence of ongoing chemical transmission. The relatively normal projections of neuronal axons and dendrites in unc- 104 also seems to argue against a defect in axonal transport. The lack of neuromuscular input to dorsal body muscles is presumed to be responsible for their occasional misdirected muscle arms. Similar misdirected muscle arms in dorsal body muscles were previously recognized as a secondary phenotype in many alleles of unc-5 and unc-6 which lack motoneuron axons in the dorsal nerve cord (Hedgecock, Culotti and Hall, in preparation). The viability of unc-104 is most encouraging; it may be feasible to do genetic studies in C. elegans of many of the proteins required for synapse formation and synaptic transmission. There are probably more genes which will produce a 'synapseless' phenotype. The paralyzed behavior and the presence of misdirected dorsal muscle arms should provide a simple means to screen for more mutants.