Why the study?
Microtubules play specialized, non-mitotic roles critical for skeletal myofiber development, function, and homeostasis, and understanding these roles clarifies how microtubule abnormalities lead to muscle disease.
Microtubules are critical for skeletal muscle development and function, and their abnormalities can lead to muscle disease.
Microtubule roles in myofiber stability warrant exploration in myopathies; leaves open validation in cardiac models.
The contractile cells of skeletal muscles, called myofibers, are elongated multinucleated syncytia formed and maintained by the fusion of proliferative myoblasts. Human myofibers can be hundreds of microns in diameter and millimeters in length. Myofibers are non-mitotic, obviating the need for microtubules in cell division. However, microtubules have been adapted to the unique needs of these cells and are critical for myofiber development and function. Microtubules in mature myofibers are highly dynamic, and studies in several experimental systems have demonstrated the requirements for microtubules in the unique features of muscle biology including myoblast fusion, peripheral localization of nuclei, assembly of the sarcomere, transport and signaling. Microtubule-binding proteins have also been adapted to the needs of the skeletal muscle including the expression of skeletal muscle-specific protein isoforms generated by alternative splicing. Here, we will outline the different roles microtubules play in skeletal muscle cells, describe how microtubule abnormalities can lead to muscle disease and discuss the broader implications for microtubule function.
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Lucas et al. (2023) studied this question.
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