Worm Breeder's Gazette 9(1): 75
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 all display a strikingly similar phenotype: XX animals are severely affected whereas there is no visible phenotype in XO animals. Mutations in dpy-21 cause recessive dumpiness in XX animals, mutations in the other three cause, in addition to an XX-specific recessive dumpy phenotype, a maternal effect XX-specific lethality. These phenotypes have been interpreted as a disruption of dosage compensation in XX animals,leading to a general increase of X-linked gene expression in XX animals. Biochemical evidence (Meyer and Casson) suggests that this interpretation is valid, at least for the genes dpy-21, nWe have developed a morphological assay to detect changes in X-linked gene expression in these animals. As originally described at the 1985 Cold Spring Harbor C. we used lin-14(n179), an apparently hypomorphic temperature sensitive mutation which leads, at the restrictive temperature, to the precocious production of adult alae during the third larval molt. The assay can be quantitated by scoring the production of alae by the 12 midbody seam cells in hermaphrodites ( 10 in males). A reduction in lin-14(n179) expression would be reflected by an increase in the number of seam cells producing precocious alae, an increase in expression.would be reflected by a reduction in the number of seam cells producing precocious alae. Indeed we can significantly increase the number of seam cells producing alae in isothermally raised XX animals by halving the gene dosage: from 64/240 cells in n179/n179 (2 copy) animals to 228/240 cells in n179/nDf19 (1 copy) animals. We have observed a dramatic suppression of precocious alae formation in XX hermaphrodites homozygous for both lin- 14(n179) and mutations in dpy-21, n[See Figure 1] The non-chauvinistic dumpy mutation dpy-6(e14) mutation has no effect on lin-14(n179) expression in this assay, indicating that the suppression seen is not simply a consequence of being dumpy. Analysis of animals in the L4 molt, reveals that over 95% of the seam cells in all the strains produced alae, showing that suppression is not simply due to an inability of these strains to produce alae. In the corresponding XO animals we see no suppression, and perhaps some enhancement, of the mutant phenotype. [See Figure 2] Thus we show that mutations in dpy-21, ects on lin-14(n179) expression consistent with their predicted involvement in dosage compensation. As an additional characterization of the functioning of these genes we have investigated the interactions between mutations at these loci. We constructed pairwise combinations of these mutations and have scored the resulting strains for viability and phenotype. [See Figure 2] The double mutant strains are no dumpier than the relevant single mutants. This lack of additivity suggests that these genes are involved in a common process, and that a mutation in any one of these genes is sufficient to disrupt this process such that mutations in the others genes have little additional effect.
