Genes of tropomyosin, troponin T, C have been known as
lev-11,
mup-2 and
pat-10, respectively. We determined the mutation sites of the tropomyosin gene,
tmy-1(
lev-11) and troponin C gene
tnc-1(
pat-10) by PCR using single worm. The tropomyosin mutation
lev-11(
st557) of Pat phenotype was in the splice site of exon 1 and caused termination. Two of three isoforms of
tmy-1 were expressed in the body walls under the control of the 5'UTS and alternative splicing of exon nine1. Charge reversion in the conserved region E163K was a reason of levamisole resistant phenotype of the tropomyosin mutation in
lev-11(
x12). Tropomyosin of the mutant worm can alternatively interact to troponin molecules and mutant worms could continue to move even in the presence of levamisole. Two mutations in the
pat-10(
st575) allele were in the second calcium binding site and in the C-terminal H-helix. The mutation D64N of troponin C caused loss of mobility shift in the presence of calcium on SDS-PAGE. Another mutation W153 termination in the H-helix may be the reason of unstable interaction to other troponin molecules. These results on the muscle proteins show that the body wall muscle function is essential for late embryogenesis of the worm. 1; Kagawa et al., (1995) J. Mol. Biol. 251, 603-613