Worm Breeder's Gazette 11(3): 52
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.
The genes dpy-26, viously been shown to be required for proper dosage compensation in XX animals. Mutations in any of these genes cause an incompletely penetrant maternal-effect XX-specific lethality due to disruption of the hermaphrodite mode of dosage compensation (Hodgkin MGG 192: 452 1983, Meyer and Casson Cell 47:871 1986, Meneely and Wood Genetics 117:25 1987, DeLong, Casson and Meyer Genetics 117:657 1987. Plenefisch, DeLong, and Meyer Genetics 121:57 1989). We have recently isolated yet another gene, dpy(y130), that appears to be a member of this family of dosage compensation genes. dpy(y130) was isolated in a xol-1 suppressor screen (Miller, et al Cell 55:167 1988) looking specifically for mutations that result in a maternal effect rescue of the xol-1 XO-specific lethality. dpy(y130) maps to the sma-1 on LGV. Homozygous dpy(y130) XX progeny of heterozygous mothers exhibit a temperature-sensitive phenotype. At 25 C, these animals are generally slightly Dpy, Egl, and Pvul. At 15 C, they appear wild type. The zygotic phenotype at 25 C appears to be similar for y130/Df1 animals. When y130 him-5(e1490) males are mated with ctDf1/nT1 unc(n754dm) hermaphrodites at 25 C, the non-Unc outcross progeny are viable and appear slightly Dpy, Egl, and Pvul. In contrast, homozygous dpy(y130) XX progeny of homozygous mothers display a temperature-sensitive lethality (see table). At 25 C or 20 C, most of these animals die before hatching or arrest as L1 larvae, with a small number of animals persisting through later larval stages before dying. The 25 C lethal phenotype is also seen in the progeny of y130 him-5(e1490)/ctDf1 mothers. This complete lethality is unusual: animals mutant in dpy-26, dpy-27, or dpy-28, always give rise to small number of dpy escapers. This does not appear to be the case for dpy(y130). At 15 C, the same terminal phenotypes are seen. In addition, a small number of fertile Dpy escapers are present. In order to determine the null phenotype of dpy(y130) we have isolated new alleles on the basis of their failure to complement the y130 zygotic phenotype at 25 C. This screen should allow us to obtain null alleles since y130/ctDp animals are viable in this generation. We have screened approximately 6500 haploid genomes and have recovered three new EMS-induced alleles of this gene. These alleles, y185, y186, and y187, also fail to complement ctDf1 and exhibit an XX-specific, maternal-effect lethality similar to y130. Interestingly, each of the new alleles appears to be temperature-sensitive for both the zygotic and maternal phenotypes. None of the alleles tested appears to be suppressible by the tRNA amber suppressor sup-7(st5) at 20 C or at 22. 5 C. [See Figure 1] In order to better characterize the nature of the dosage- compensation defect associated with dpy(y130 etc), we have performed reconstruction experiments to determine the degree to which these alleles will rescue xol-1 XO dead animals. Preliminary results indicate that fewer than 1% of dpy; xol-1 XO homozygotes are rescued if their mother is dpy/+. A far greater number of dpy; xol-1 XO progeny are rescued if the mother is homozygous for the dpy mutation. The rescued animals exhibit a broad range of sexual phenotypes extending from fertile hermaphrodites to males. In contrast to the other maternal-effect dpy genes, dpy(y130, y185, y186, y187) appears to rescue xol-1 XO animals well only if both the mother and her progeny are mutant. This may reveal a qualitative or quantitative difference in this gene's role in the dosage compensation process. We have also begun to clone this new gene. dpy(y130) lies on the her-1 contig between the cloned loci act-1, 2, 3 and myo-3. We have identified RFLPs in wild C. elegans strains between these markers, and we are in the process of mapping these polymorphisms with respect to dpy(y130) in order to pinpoint its position on the contig.