Worm Breeder's Gazette 8(3): 49

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.

ced-4(III), a Second Gene Involved in the Initiation of Programmed Cell Death

H. Ellis, C. Desai, R. Horvitz

We have previously shown that the wild-type function of ced-3 IV is 
required for the initiation of programmed cell deaths.  We have now 
identified a second gene, ced-4 III, that also is required for the 
initiation of programmed cell deaths.  ced-4(n1162) was isolated as a 
suppressor of the egg-laying defect of egl-1(n1084) hermaphrodites.  (
egl-1 hermaphrodites are egg-laying defective because the HSN neurons, 
which are required for normal egg-laying, die during embryonic 
development.)  ced-4; odites, like ced-3; 
odites, have HSNs and lay eggs normally.  
From our preliminary observations the phenotype of ced-4 animals 
appears very similar to that of ced-3 animals.  However, ced-4 maps on 
LGIII between unc-79 and dpy-17 and complements ced-3 mutations.  Like 
ced-3 animals, ced-4 animals are missing cell deaths, have an extra 
dopaminergic neuron in each postdeirid, and an extra NSM on each side 
of the pharynx; like ced-3 hermaphrodites, ced-4 hermaphrodites have 
neurons that appear by their positions and morphologies to be 
indistinguishable from the normally male-specific cephalic companions. 
Animals of genotype ced-4(n1162); 7) appear 
equivalent in phenotype to either mutant alone.  So far we have found 
ced-4(n1162) to differ from ced-3 mutations in only one respect: 
whereas ced-3 mutations are semidominant suppressors of the egg-laying 
defect of egl-1 heterozygotes, ced-4/+; are 
not suppressed.