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.
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 mating.