Worm Breeder's Gazette 10(2): 23
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.
Mutations in dpy-21, dpy-27, and dpy-28 cause XX animals to be dumpy and/or inviable, while XO animals remain essentially unaffected. It has been demonstrated that these mutations result in the over-expression of X-linked genes in XX animals (Meyer and Casson Cell 47:871 1986, Meneely and Wood Genetics 117:25 1987, DeLong, Casson and Meyer Genetics 117:657 1987). Recently we have discovered a powerful screen for the isolation of mutations in genes, such as dpy-21, dpy-27, and dpy-28, that are involved in the execution of the hermaphrodite mode of dosage compensation. Mutations in xol-1 cause the aberrant invocation of the hermaphrodite mode of dosage compensation in XO animals; the resulting under-expression of the single X chromosome in these animals causes them to die as embryos (see L. Miller, WBG v10 n1; L Miller, this WGB) . Mutations which disrupt the hermaphrodite mode of dosage compensation result in the rescue of xol-1 XO animals. By reverting the xol-1 XO lethality we isolated mutations in a number of genes that are required for the proper execution of the hermaphrodite mode of dosage compensation. Among the many suppressors isolated were 14 new alleles of dpy-21 (3 of which are suppressible by sup-7(st5), and another 2 of which were isolated in a mutator strain), 1 new allele of dpy26, and 5 new alleles of dpy-27 (1 of which is suppressible by sup- 7(st5)). In addition, we isolated a single allele of a new gene, dpy- 29, which maps to the unc-61 of LG V. Homozygous dpy-29(y100) XX progeny of heterozygous mothers are dumpy; homozygous progeny of homozygous mothers are inviable, with rare dumpy escapers. This lethality is cold sensitive: at 20 C the viability of XX animals in homozygous dpy-29(y100) strains is 3.4%; at 15 C it is 0.6%. XO animals appear unaffected. By the lin-14 assay, we have shown that dpy-29(y100) suppresses the lin-14 phenotype in XX animals to a degree equivalent to that seen with dpy-21, dpy-27, or dpy-28 mutations. In dpy-29 this suppression is seen in the homozygous progeny of heterozygous mothers. No suppression is seen in dpy-29 XO animals. Thus dpy-29(y100) results in sex-specific over-expression of X-linked genes. The phenotypes of dpy-29 are essentially identical with those seen in dpy- 27, in that dpy-29(y100) does not promote X-chromosome nondisjunction as do mutations in dpy-26 and dpy-28. We have previously constructed dpy-27; dpy-28; dpy-28 double mutant animals, and shown that these animals are about as viable as the single mutants. Preliminary results from the construction of dpy-27; dpy-29 suggest that these animals are also about as viable as the single mutant. We interpret this to mean that dpy-29, as well as dpy-26, involved in a common process, which we believe to be the execution of the hermaphrodite mode of dosage compensation. Finally, given the number of alleles of these genes in existence, it is possible that additional genes in this class exist. Thus we are continuing our xol-1 XO reversion screen to identify both more alleles of dpy-26, dpy-28, and dpy-29 as well as any additional new genes in this class.