Worm Breeder's Gazette 12(5): 69 (February 1, 1993)
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.
Shared genetic programs between the embryonic DD and postembryonic VD motoneurons (mns), collectively called the D mns, are responsible for the morphological and neurochemical similarities between the two classes. Less is known about the genetic basis for such distinctions, in that the DD and VD mns have opposite patterns of synaptic inputs and they have different lineal origins. Excluding mutations in genes that disrupt the lineages of the postembryonic mns, unc-55 is the only gene that specifically effects one D mn class and not the other (Nawrocky and White, personal communication). Interestingly, unc-55 ,causes the VD mns to adopt the same synaptic pattern as the DD mns; thus ventral inhibitory synapses are removed and relocated to the dorsal cord. The ventral coiling behavior of unc-55 mutants correlates well with either or both of these changes.
Varicosities associated with the accumulation of synaptic vesicles in presynaptic sites of neuromuscular junctions are commonly observed in C. elegans motoneurons. The dorsal branches of the D mns of unc-55 mutants should be composed entirely of presynaptic branches possessing varicosities and the ventral cord should have only smooth postsynaptic branches. A light level immunohistochemical investigation comparing the morphology of D mns in wild-type and unc-55 mutants was undertaken to determine whether an anatomical correlate existed for the alteration of the synaptic patterns in the VD mns. This was done using a commercially available antibody to the D mn transmitter GABA.
In the unc-55 mutants the number of varicosities observed as changes in the caliber of the processes appears to increase in the dorsal cord and was reduced in the ventral cord when compared to wild type. This correlated with our expectations but the differences were not robust. Recently we have begun to analyze these preps with confocal microscopy and hopefully the results will be clearer. Both mutant alleles e402 and e1170 have the normal complement of 19 cell bodies in the ventral nerve cord. In 5% of the unc-55 animals the cell body of VD7 was displaced laterally and a process returning to the ventral cord was visible. Less frequently, the commissure of the VD13 travelled around the wrong side of the animal to reach the dorsal cord. No defects have been observed in any of the DD mns.