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We incorporated morphological and microtubule architectural concepts into a simplified finite element mathematical model of myofiber mechanics, which suggests a greater contribution of myofiber morphology than microtubule structure to muscle biomechanical performance. microtubule architecture in the underlying susceptibility to injury seen in dystrophic muscles. In addition, we studied malformed MDX myofibers to better understand the role of altered myofiber morphology vs. Previous studies established that microtubule structure at the cortex is disrupted in MDX myofibers our analyses extend these findings by showing that microtubule structure in the core is also disrupted. MDX nuclei also showed altered transcriptional activity. MDX muscle shows reduced expression and labeling intensity of nesprin-1, a LINC protein that attaches the nucleus to the microtubule and actin cytoskeleton. Nuclei in MDX myofibers were more mobile than in WT myofibers for both distance traveled and velocity. Because movement of nuclei is not only LINC dependent but also microtubule dependent, we analyzed microtubule density and organization in WT and MDX myofibers, including the application of a unique 3D tool to assess microtubule core structure. We also examined expression of proteins in the linkers of nucleoskeleton and cytoskeleton (LINC) complex, as well as nuclear transcriptional activity via histone H3 acetylation and polyadenylate-binding nuclear protein-1.

We examined nuclear movement in wild-type (WT) and muscular dystrophy mouse model for DMD (MDX) (dystrophin-null) mouse myofibers. Although the genetic basis is known, the pathophysiology of dystrophic skeletal muscle remains unclear. Duchenne muscular dystrophy (DMD) is a genetic disorder in which the absence of dystrophin leads to progressive muscle degeneration and weakness.

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