Worm Breeder's Gazette 11(4): 108

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.

Genes Affecting Axonal Guidance of Different Classes of Neurons

Shahid Siddiqui

Figure 1

I have previously reported (e.g.  CSH meetings 1985, 1987, 1989) 
several monoclonal and polyclonal antisera that can be used to 
specifically label different subsets of identified neurons in C.  
elegans.  Here I wish to report a comparison of axonal guidance 
defects as observed in the set of unc mutants (Brenner, 1974) by 
immunocytochemical staining of whole animal squash preparations.  For 
mutants in every gene several alleles (where available) were stained.  
I have included only those genes for which the penetrance of the 
axonal defect was at least 15%; e.g.  unc-18 worms show abnormal touch 
cells, but it is not included here, since the defect is observed in 
only about 10% stained worms.
[See Figure 1]
Desai et al.  (l988) have described mutants in eight of the above 
mentioned genes (unc-6, unc-33, unc-34, unc-40, unc-51, unc-71, unc-73,
and unc-76) affected in the axonal guidance of HSN neurons.  
I have termed 'abnormal' to denote any deviation in neuronal cell 
body position, axonal outgrowth and or process placement, from the 
normal pattern observed in the wild type.  
Our results suggest that in C.  elegans, sensory and motor neurons 
require the combined activity of a large number of genes: genes that 
affect the generation of migration of neurons and genes that axonal 
growth and process placement, i.e.  the neural circuitry is a result 
of concerted activity of a group of genes that are required in more 
than one neuronal type.  In addition, I find that these mutants show 
great variability in expressivity and penetrance of axonal defects, 
although the locomotory defects are very strong.  It is likely, that 
some of the defects observed in axonal growth are caused by secondary 
defects in non-neural tissue, including hypodermis and muscle.  
Leakiness of a mutation may also cause variability of the axonal 
defect.  Temperature sensitive alleles of these mutations may provide 
a correlation between behavioral alterations and changes in neural 
circuitry.  Apparently there are very few genes that affect only one 
class of neurons selectively; even if such genes are discovered, the 
phenotype may simply reflect a differential requirement for the gene 
I would like to thank, J.  Culotti, M.  Chalfie, R.  Durbin, E.  
Hedgecock, R.  Horovitz, S.  McIntire, J.  Sulston, and J.  White, for 
many useful discussions.  I thank J.  Culotti, R.  Holmgren and J.  
Miwa for support and encouragement.

Figure 1