Key result
Mutations in the troponin C gene pat-10 of C. elegans, which alter calcium and troponin I binding sites, lead to developmental arrest as twofold paralyzed embryos.
The troponin C gene pat-10 is essential for proper muscle function during development in C. elegans, with specific mutations disrupting calcium and troponin I binding.
Animal data on pat-10 do not change clinical practice; leaves open its value as a model for vertebrate cardiac troponin C.
We have cloned and characterized the troponin C gene, pat-10 of the nematode Caenorhabditis elegans. At the amino acid level nematode troponin C is most similar to troponin C of Drosophila (45% identity) and cardiac troponin C of vertebrates. Expression studies demonstrate that this troponin is expressed in body wall muscle throughout the life of the animal. Later, vulval muscles and anal muscles also express this troponin C isoform. The structural gene for this troponin is pat-10 and mutations in this gene lead to animals that arrest as twofold paralyzed embryos late in development. We have sequenced two of the mutations in pat-10 and both had identical two mutations in the gene; one changes D64 to N and the other changes W153 to a termination site. The missense alteration affects a calcium-binding site and eliminates calcium binding, whereas the second mutation eliminates binding to troponin I. These combined biochemical and in vivo studies of mutant animals demonstrate that this troponin is essential for proper muscle function during development.
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Terami et al. (1999) studied this question. pat-10 gene mutation was evaluated. Mutations in the troponin C gene pat-10 of C. elegans, which alter calcium and troponin I binding sites, lead to developmental arrest as twofold paralyzed embryos.
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