Worm Breeder's Gazette 11(3): 72
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.
In unc-52 mutants movement is normal throughout the early larval stages, but the worms become progressively paralyzed as they age. The onset of paralysis can begin as early as the L3 stage, or may not begin until after the final larval molt, depending upon the allele. At the cellular level, paralysis is correlated with the disruption of the normal oblique striations of the muscle fibers in the body wall muscle cells. In completely paralyzed worms the birefringence in the muscle cells is very patchy and unstructured when viewed under polarized light. In order to learn more about the role of unc-52 in maintaining normal muscle structure, we have been screening for reversion of the paralyzed phenotype. Since the dense body is affected by mutations in unc-52, hopefully, some of the suppressors we have isolated will identify genes involved in the formation or maintenance of this structure. A total of 44 revertants have now been isolated from 12 EMS mutagenesis screens and one screen for spontaneous revertants ( ~10+E7 animals per screen). Two spontaneous revertants have also been found on stock plates. Eighteen of the 35 strains analyzed have proven to be intragenic revertants which vary in phenotype from poorly moving (but better than unc-52) to almost wild type. The remaining 17 strains are extragenic suppressors of unc-52 and are similar in phenotype to the intragenic revertants. None of the suppressor mutations appear to confer a phenotype on their own. Six of the extragenic suppressors have been mapped, and all are on LGIV near dpy- 4. This suggests that they may define a single gene. One of these mutations suppresses all of the muscle-affecting unc-52 alleles, but the allele specificity of the other suppressors has not yet been determined. At the cellular level, most of the body wall muscle cells in well- moving, suppressed worms look wild-type, but some single cells show a slight patchiness which appears to result from the filaments detaching from the cell membrane. Because movement is completely normal in some of these worms, the disruption of the normal striated pattern in the muscle cells may be due to stress during preparation for viewing under the microscope. In wild-type worms this type of disruption is not seen, suggesting that suppression of unc-52 by these secondary mutations is not complete.