Worm Breeder's Gazette 1(2): 14

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.

Egg-laying Deficient Mutants

B. Horvitz, J. Sulston

Mutants of C.  elegans which do not lay eggs end up as 'bags of 
worms'.  Progeny hatch internally and devour their parent; the 
residual adult cuticle encloses about 50 active young larvae.  
Eventually, these larvae crawl free of the cuticle.
Because of its striking phenotype, a bag of worms is easy to detect 
on a plate containing F2 progeny of mutagenized nematodes.  In 
addition, bags of worms are of lower density than living nematodes and 
can be isolated by centrifugation in a Ficoll step gradient.  (At 4 C, 
bags of worms float and living worms pellet in 16 per cent w:w Ficoll,)
Using these techniques, 57 mutants have been isolated from among 
approximately 15,000 independent F2 progeny produced by EMS-
mutagenized worms.  All mutants which have been examined appear to 
produce bags of worms because of deficiencies in egg-laying.
We have begun to characterize both these mutants and similar egg-
laying deficient mutants isolated by others.  Many mutants have proved 
to have abnormal post-embryonic cell lineages (see Worm Breeders' 
Gazette, Vol.  1, No.  1).  Virtually all of these cell lineage 
mutants show variable penetrance.
Three mutants (E1309, dev-2 X; E1417, dev-3 IV; E1413, II) appear to 
be specifically blocked in the divisions of the ventral hypodermal 
cells which produce the vulva.  No eggs can be laid because no vulva 
is present.  Males of these strains appear essentially normal and are 
capable of mating.
E912, rep-2 II, isolated by Babu and previously examined by Jonathan 
Hodgkin, is also defective in the ventral hypodermal cell lineages.  
Other lineages (such as those which produce the posterior lateral 
ganglia) are affected as well.  Males are grossly abnormal and 
incapable of mating; most, if not all, male-specific cell lineages are 
defective.  some cells in the male undergo extensive proliferation, 
leading to hundreds of extra cells in the tail region and, generally, 
to the death of the animal.
Mutations in two genes -- unc-83 V (2 alleles) and unc-84 X (4 
alleles) -- prevent the migrations of the ventral cord precursor 
nuclei into the ventral cord.  Because these precursors normally 
generate the ventral hypodermal cells involved in vulva formation, 
these mutants fail to form vulvae.  In addition, they are behaviorally 
uncoordinated because of their ventral nerve cord defects.  The dorsal 
hypodermal ridge of a nuclear migration mutant contains nuclei of the 
hypodermal syncytium (In N2, this ridge is normally devoid of nuclei.).
This defect is visible as early as the 'comma-stage' of 
embryogenesis; conceivably, the resulting hypodermal abnormality may 
be the reason for the subsequent deficiency in the migrations of the 
nuclei of the precursor cells located in the subventral hypodermis.  
Males of these strains fail to mate.  All six alleles of these two 
genes are temperature sensitive.
E1414, unc-85 II, shows blocks in late divisions in the ventral 
nerve cord cell lineage and is behaviorally uncoordinated (see White 
et al., this newsletter).  Other lineages, such as those which produce 
the posterior lateral ganglia, are also affected (see Dew and Sulston, 
this newsletter).  It is not known why this mutant fails to lay eggs.  
Males show gross deficiencies in their rays and are incapable of