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.
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.