Worm Breeder's Gazette 11(4): 55
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.
lin-34 mutations can cause a dominant Multivulva (Muv) phenotype, while let-60 mutations can cause dominant Vulvaless (Vul), recessive lethal or recessive Vul/lethal phenotypes. lin-34 and let-60 are likely to be the same gene because they map very close together and the tightly linked lin-34(n1046) suppressor n1981 is a recessive lethal mutation that fails to complement let-60 mutations. Preliminary molecular data are consistent with this interpretation ( Min Han and Paul Sternberg, personal communication; also our unpublished observations). We investigated the nature of the dominant Muv and dominant Vul alleles using a new duplication of chromosome IV, nDp5. Isolated by Saechin Kim, nDp5 appears to be a free duplication that spans lin-34/let-60 and extends from at least unc-44 to unc-26, covered. Using this duplication and a deficiency that spans the lin-34/let-60 region, we constructed strains containing varying doses of the wild-type and mutant alleles. As seen in the table below, the dominant Muv mutations n1046 and n1700 show an increasingly severe phenotype with increasing copies of the wild-type gene. This result suggests that these mutations cause an increase in a wild-type-like gene activity and are therefore hypermorphic mutations. The dominant Vul mutations n1631 and n2031 seem to antagonize the wild-type gene activity and thus are antimorphic mutations. However, the dominant Vul mutations are not able to antagonize the activity of the dominant Muv mutations, since dominant Muv/dominant Vul heterozygotes have the same phenotype as dominant Muv/+ heterozygotes. Since nDp5 appears to be a free duplication that is lost at a fairly high rate during meiosis, we will attempt to do mosaic analysis of the lin-34/let-60 locus using nDp5.[See Figure 1]