Worm Breeder's Gazette 5(1): 12
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.
Indirect suppression of thick filament muscle defects (unc-54 and unc-15) was reported by Riddle and Brenner (Genetics 89: 299-314, 1978) . The discovery in Bob Waterston's laboratory that a suppressor- carrying strain unc-541 (e675); sup-3V (e1407) overproduces non-unc-54 myosin heavy chains lends strong support to the hypothesis that the sup-3 gene is involved in regulation of myosin gene expression. The sup-3 mutations apparently compensate for unc-54 mutations by increasing the level of non-unc-54 myosins in muscle cells. Suppression of unc-15 (e73) could be explained if e73 paramyosin is better able to assemble with the non-unc-54 myosin. Our working hypothesis, based primarily on genetic data, is that sup-3 may be a repressor gene. We are attempting to use suppression to identify additional muscle genes, especially the structural gene (or genes) which may be under sup-3 control. Mutations in such a gene would prevent suppression. Six mutations which interfere with suppression have been partially characterized. These derivatives of unc-15 (e73); sup-3 (e1407) were picked as paralyzed (e73-type) individuals in the F1 and F2 progeny of EMS-treated worms. One of the derivatives appears to carry a dominant mutation, unlinked to either unc-15 or sup-3, and related to suppression. Dominance was determined by mating the mutant with unc- 15, ne half of the male progeny being paralyzed. The relationship to suppression was determined by mating the mutant with N2 males. L4 hets were cloned and their progeny counted. The presence of a suppressed (slow) class of progeny indicated that this mutation is unlinked to unc-15 and sup-3. If it were linked to either gene, the frequency of suppressed progeny segregated would be decreased. The ratio of unc to wild-type progeny indicated that this mutation is related to suppression, and does not exhibit a paralyzed phenotype by itself. Two other mutations also appear to be unlinked to unc-15 or sup-3, exhibit no mutant phenotype of their own, but are recessive. The differences in dominance may reflect quantitative differences in the reduction of non-unc-54 myosin. Since sup-3 mutations approximately double the amount of non-unc-54 myosin, suppressor activity presumably can be eliminated by a 50% reduction in that amount as would occur in a null /+ heterozygote.