Caenorhabditis elegans, a well-known research animal model, has also become a robust model for studying muscle structure and function in vivo. Their body wall muscles are functionally analogous to vertebrate muscle, as they include dense bodies and M-lines, the former being functionally equivalent to vertebrate Z-lines. The number of proteins known to be located in dense bodies and M-lines is increasing and the role of many are not well understood, particularly with regards to the development and maintenance of muscular strength. C. elegans, along with our NemaFlex apparatus that enables muscle strength measurements, offers an extremely powerful platform to study genes impacting muscle strength. We have studied mutations of specific genes that encode proteins known to localize to each muscle structural category: dense body, M-line, and dense body and M-line together. In our initial investigation, we have chosen
unc-82 and
unc-89 mutants (strains CB1220 and CB1460, respectively) that have defects in M-line structure,
uig-1 mutants (strain RB978) that affect the dense body and
zyx-1 mutants (strain VC299) that affect both the dense body and the M-line. Strength measurements were performed using the NemaFlex, which consists of force-sensing micropillars. Our results show that some of the mutants were weaker in strength, but others interestingly did not show discernible strength difference.
unc-89 and
zyx-1 animals showed a significant decrease in strength, while
uig-1 and
unc-82 did not.
unc-89 animals were the weakest likely due to the fact that these mutants are reported to be missing the M-line. On the other hand, mutations in
uig-1 and
unc-82 did not result in strength discernible from wild-type indicating that they may not have a key role in force generation. This could be due to the fact that the protein products of these genes are reported to have a signaling function instead of a structural role in muscles. These initial studies lay the groundwork for a high-throughput screen of muscle-related genes that can help to identify the key muscle proteins impacting strength. This knowledge can help identify targets for disease therapies involving muscle dysfunction including muscular dystrophy, cachexia and dynapenia.