Worm Breeder's Gazette 10(3): 10
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.
dpy-21 appears to be required in both XX and XO animals for proper dosage compensation. In XX animals, mutations in dpy-21 result in a Dpy phenotype and elevated X-linked gene expression. XO dpy-21 animals appear wild-type in length, but they also have altered X- linked gene expression. To date dpy-21 is the only XX specific dpy mutation that appears to affect both XX and XO animals. We have begun a systematic genetic analysis of dpy-21. The mutant phenotype of dpy-21 was originally defined by the alleles e428 and e459 (J. Hodgkin, Mol. Gen. Genet. 192: 452 (1983). 12 new EMS induced alleles have been isolated as suppressors of the XO-specific lethality of xol-1(y9). Three of these alleles (y47am, y59am and y60am) are suppressible by sup-7(st5) X. All alleles isolated to date resemble the original alleles: XX animals are Dpy, frequently have a protruding vulva (rare animals are Bivulva) and occasionally are Egl. XO animals appear wild-type. In five of six alleles tested for viability at 20 C the progeny of homozygous mothers have reduced viability: e428 (83%), y47am (86%), y58 (96%), y60am (89%), y87 (93%) ( percent of zygotes that matured to adulthood). The exception is y88ts, which is slightly Dpy at 15 C, Dpy and fully viable at 20 C (99.8%), and Dpy with reduced viability at 25 C (90%). Despite the isolation of amber suppressible alleles, it is possible that null alleles of dpy- 21 might not have been recovered from the xol-1 suppression screen. We have devised a complementation screen that has allowed the isolation of deficiencies of dpy-21 and we are now using this same screen to isolate additional EMS induced alleles of dpy-21.Using the complementation screen we have isolated 3 gamma ray induced mutations ( yDf4, yDf6 and yDf7) that fail to complement both dpy-21 and par-4( it57), which lies to the right of dpy-21. Since all three deficiencies complement mutations to the left of dpy-21, we must use molecular markers to show that the deficiencies do indeed span the dpy- 21 locus. The 5S rRNA contig, which maps just to the left of dpy-21, will provide the initial probes for mapping the leftmost deficiency endpoints. dpy-21(y88ts)/yDf6 hermaphrodites are Dpy and 70% viable ( compared to 99.8% viability for y88/y88). In contrast, the viability of dpy-21(y88ts)/yDf4 and dpy-21(y88ts)/yDf7 hermaphrodites is reduced to 14% and 20%, respectively. The severely reduced viability in these two stains may be explained in part by the additional mutant phenotypes associated with these two deficiencies. yDf4/unc-76 and yDf7/unc-76 strains produce 35% and 41% dead eggs respectively and only 17% of zygotes mature to become Unc-76 hermaphrodites. Since both deficiencies have been multiply backcrossed these results may indicate that yDf4 and yDf7 have some dominant maternal-effect lethality. In addition, Df/unc-76 hermaphrodites are slow growing ( evidence of haploinsufficiency). Our working hypothesis is that all three deficiencies span the dpy-21 locus and that the dominant effects of yDf4 and yDf7 are due to removal of some other locus or loci. To determine if the available dpy-21 alleles are null we compared the viability of y88ts/yDf6 (70%) to that of y88ts/y60am (94%). In this situation y60am does not act like a null allele, in that it does not resemble a deficiency when placed in trans to a hypomorphic allele. Two possible interpretations of these data are: 1) we have not yet isolated a null allele of dpy-21 or 2) yDf6 removes a locus that acts synergistically with dpy-21. This question will be settled once we know the nature of mutations obtainable from the complementation screen.