Mutants with abnormal muscle can be readily recognized from this point onwards by their reduced movement and abnormal muscle structure. More than 40 genes have been identified, and a major challenge has been to determine what these genes encode and how they function in normal muscle. At present, genes for actin, myosin heavy and light chains, paramyosin tropomyosin and actin capping proteins have all been identified, and structure-function relationships can be analyzed in detail. Some of these proteins also function in cytoplasmic motility and are implicated in key developmental processes. The mutants together with antibodies raised against many of the components have defined an assembly pathway.
Initial events occur at the muscle cell membrane with the integrins playing a central role.
Surprisingly, the overall striated pattern depends primarily on these membraneassociated events and not on the actin or myosin filaments themselves. With the implementation of automation and a significant scale up, we intend to increase sequence throughput sufficiently to complete the entire sequence by mid 1998. Interpretation of the sequence will substantially increase our knowledge of C. elegans biology and open up new avenues for investigation. Wilson, R., et al. 2.2 Mb of contiguous nucleotide sequence from chromosome III of C. elegans .