Worm Breeder's Gazette 9(2): 74
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 isolated a set of eight dominant temperature-sensitive (ts) embryonic-lethal mutations. As described previously, these could potentially include mutations at haplo-insufficient loci or in members of a redundant multi-gene family (WBG 9[1]44, 1985). Five of the mutations have been analyzed in some detail and mapped to the following intervals: ct42, unc-11--dpy-5(I); ct45, unc-69--vab-7 (III); ct46, lin-10--unc-29(I); ct59, unc-24 ); and ct60, dpy-11--vab8(V).All five mutations show a parental effect: that is, heterozygous hermaphrodites at the restrictive temperature lay more than 75% dead eggs (the maximum number expected for a dominant zygotic lethal). These effects are maternal rather than paternal, since the embryos were not rescued by mating heterozygous mutant hermaphrodites to N2 males at the restrictive temperature. Likewise, the sperm of males heterozygous for each mutation did not kill eggs from wild-type mothers (ct60 not tested). An additional recessive zygotic phenotype at the permissive temperature is seen for three of the mutations. Homozygotes for ct42 and ct45 are inviable, while homozygous ct60 animals do not produce eggs. Both ct46 and ct59 are viable as homozygotes, but their eggs show reduced hatching compared to those of heterozygotes at 16 C. This could indicate an additional recessive zygotic phenotype for ct46 and ct59 or may result from an additive effect of being homozygous for the dominant maternal-effect phenotype. None of the five mutations shows a dominant zygotic effect. Heterozygous mutant animals balanced with an appropriately marked wildtype homolog were selfed at 16 C, 20 C, and 25 C. The surviving progeny at all three temperatures were found in a 3:1 ratio of morphologically wildtype:marked animals (for ct42 and ct45, the ratios were reduced to 2:1 since both are recessive zygotic lethals). Therefore, zygotes carrying the mutation have an equal viability to homozygous non-mutant animals, and so there is no dominant zygotic lethality (or recessive lethality in the cases of ct46, ct59 and ct60). The lack of a zygotic dominant phenotype was confirmed by introducing the mutation through males. Crosses of males heterozygous for the mutations to non-mutant wild-type hermaphrodites did not result in dead eggs, and the male's mutant and wild-type alleles were passed at equal frequencies to the progeny (ct60 not tested). Preliminary gene-dosage experiments have been performed on ct42 and ct46. When heterozygous with a deficiency, both show phenotypes similar to those of the corresponding homozygotes. ct42/sDf4 is probably inviable at 16 C, while ct46/nDf24 shows reduced hatching of eggs. Neither +/sDf4 nor +/nDf24 shows any temperature sensitivity. Thus, both ct42 and ct46 must be gain-of-function alleles whose dominant effects cannot be the result of haplo-insufficiency. ct42 may be weakly rescued by a duplication of the region. Eggs of sDp2/ct42/+ animals showed 20% hatching at 25 C, compared to 13% for ct4Z/I. In addition, sDp2/ct42/ct42 animals are fully viable at 16 C, but all of their eggs fail to hatch at this temperature. We may have an additional allele of the gene represented by ct46. ct61 maps to the same interval [lin-10--unc-29(I)]. Both mutations show a similar pattern of aberrant early cleavages reminiscent of zyg- 9(II): the initial cleavage is longitudinal rather than transverse, and multiple nuclei may be present.