The small nematode Caenorhabditis elegans is the subject of intensive investigation into the genetic specification of muscle structure and function. Many mutations affecting muscle structure have been identified, and more than 20 genes have been defined by complementation and recombinational analysis. Biochemical and genetic studies have proved that one of these loci,
unc-54 I, is the structural gene for a 210,000-dalton myosin heavy chain in the body-wall musculature. Specific mutations in this gene could help us to understand the role of the myosin heavy chain in the assembly and contraction of muscle. Additional myosin heavy chains, the products of other genes, are present in the body wall and pharyngeal musculature. Alterations in the tissue-specific expression of this family of genes might be useful in studying gene regulation. The classic genetic approaches of reversion and intracistronic recombinational analysis can be applied to these problems in C. elegans because of the ease of handling the large number of animals necessary for systematic application of these methods, and because of the strong phenotype associated with most
unc-54 mutations. Reversion analysis can reveal intragenic suppressors of a variety of types and could be especially powerful in the study of the genetic specification of muscle where many gene interactions may be involved. We have, in other work, described allele-specific generalized suppressors in C. elegans that are likely to be informational suppressors. Riddle and Brenner reverted
unc-54 mutants and uncovered a gene-specific suppressor,
sup-3 V. Part of our current work has been directed toward understanding the molecular basis for
sup-3 action on
unc-54 mutants. We have also carried out reversion analysis on
unc-22 mutants and, surprisingly, have found new alleles of
unc-54 that suppress
unc-22 expression. In addition, a genetic intracistronic map of the
unc-54 gene has been constructed, and we have begun to position these new alleles on this