The cloning and mapping of the alpha-actinin gene (atn-1) in C. elegans provides a foundation for future genetic analysis of this actin-binding protein.
Cloning atn-1 equips C. elegans for targeted alpha-actinin studies; leaves open links to muscle mutations and requires functional validation.
The dense-bodies in the body wall muscle of the nematode Caenorhabditis elegans function to anchor the actin thin filaments to the adjacent sarcolemma. One of the major components of the dense-bodies is the actin-binding protein alpha-actinin. To facilitate a genetic analysis of alpha-actinin, we have cloned a cDNA encoding the nematode protein, identified its position on the nematode physical map, and developed a unique PCR based approach to test the position of the cloned gene relative to known genetic deletions. The peptide sequence deduced from the cDNA shows that, apart from a few exceptional regions, the nematode protein shows strong similarity to other known alpha-actinins. Its position on the genetic map shows that none of the known muscle affecting mutations identified in C. elegans are in this alpha-actinin gene. This gene has been given the name atn-1 (alpha-actinin-1).
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Barstead et al. (1991) studied this question.
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