We have reported in the last worm meeting that affinity purified antibodies raised against horseradish peroxidase (HRP) stain specific neurons and sensory support cells in C. elegans (indirect immunofluorescence on whole animal squashes). Mutations in 5 unc genes which lead to foreshortened PHA and PHB axons as determined by FITC uptake (Hedgecock et al. WBG vol 7 #1,
p70-71, & Culotti et al. this WBG) were analyzed immunocytochemically for their effect on the growth of nerve processes through the pre-anal ganglion (PAG). Mutants of genes,
unc-33 IV,
unc-44 IV,
unc-51 V,
unc-76 V, and unc-(
ev411)V when stained with anti-HRP antibodies show that while PHA and PHB axons are blocked in their growth through the PAG, other neuron types are not. This observation suggests that the short axon phenotype of some neurons in these mutants is not due to a nonspecific block of axon growth within the PAG. This precludes certain interpretations concerning the nature of the defects, for example, the mutants do not present some kind of a physical barrier to axonal growth within the ganglion per se, nor are they alterations in the overall organization of the PAG which might block the growth of all neurites through the ganglion. In addition to the premature termination of PHA and PHB axons in mutants of
unc-51, staining with anti-HRP antibodies revealed that in a fraction of
unc-51 (
e369) animals nerve fibers abnormally emanate from the lumbar ganglia, fail to reach the ventral nerve cord, and instead run in various lateral positions. Therefore, although the PHA and PHB axons show normal growth to the posterior end of the PAG, other neurons in the lumbar ganglia are misguided in
unc-51 animals. Moreover, in some
unc-51 (
e369) animals, nerve fibers could be seen to exit from the ventral cord, wander aimlessly, and terminate randomly. These observations are consistent with the finding that the post- deirid neuron (PDE) in
unc-51 mutants can also show guidance defects ( Ed Hedgecock, Joe Culotti, and Liz Perkins, unpublished).