C. Elegans Model for Studying Tropomyosin and Troponin Regulations of Muscle Contraction and Animal Behavior

Abstract

There are two muscle tissues in the nematode Caenorhabditis elegans: the pharynx for feeding and the body wall for locomotion. These correspond to cardiac and skeletal muscles in vertebrates, respectively. Study of the muscle genes of C. elegans can be classified into three stages; first, mutant isolation and gene mapping, second, cloning and sequencing of the gene, and third, complete sequences of all genes. Many uncoordinated mutant animals have been isolated (Brenner, 1974; Waterston, 1988; Moerman and Fire, 1997) and the complete amino acid sequence of myosin heavy chain, twitchin, and paramyosin, (invertebrate specific core protein of thick filament), and were the first determined in any animals by analyzing the unc-54, unc-22, and unc-15 mutants, respectively (Karn et al., 1983; Benian et al., 1989; Kagawa et al., 1989). Tropomyosin and troponin components are also present but as with actin and myosin heavy chain in the worm, there are some differences in gene structure and sequence compared to those in other animals (Kagawa et al., 1995; Myers et al., 1996; Moerman and Fire, 1997). Deficiencies of body wall troponin C or tropomyosin in C. elegans cause the Pat (paralyzed arrest at embryonic two-fold stage) phenotype (Williams and Waterston, 1994; Terami et al., 1999) and those of troponin T cause Mup (muscle position abnormal) phenotype (Myers et al., 1996). After determining the complete genome sequences of the nematode (The C. elegans Sequence Consortium, 1998), we can find out how isoforms are related to each other. Only one troponin C gene, pat-10/tnc-1, is expressed in the body wall muscles and the gene defect causes a developmental arrest of the animals (Terami et al., 1999).