Abstract
Little is known about the molecular basis for differential gene expression during muscle development, the assembly of contractile proteins into filament lattices, or the functions of contractile protein isoforms in different muscle tissues. The small soil nematode Caenorhabditis elegans is an attractive organism in which to apply biochemical and genetic approaches to the study of these problems. Only two major muscles are present in the organism—the pharyngeal muscle and the body wall muscle—and the anatomy and lineage of all the muscle cells in the organism throughout development are known (Suiston et al, 1983; Suiston and Horvitz, 1977). Because a large fraction of the nematode tissue mass is muscle, the major contractile proteins can be isolated in milligram quantities from a few liters of nematode culture (Epstein et al, 1974; Waterston et al, 1977; Harris and Epstein, 1977; MacLeod et al, 1977a,b; Zengel and Epstein, 1980c). Caenorhabditis elegans exhibits a characteristic swimming pattern on the surface of agar plates. Genetic analysis (Brenner, 1974) has defined mutations in more than 100 different genes that produce animals with defective motility (the uncoordinated, or unc, phe-notype). Mutations in 22 of these unc genes create gross abnormalities in muscle ultrastructure (Waterston et al, 1980; Zengel and Epstein, 1980b).
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