Activity-Dependent Sarcomere Remodeling in C. elegans Muscle Correlates with Mechanical Vulnerability in Dystrophy.

Sarcomere networks (formed by lateral connections between myofibrils) are essential for force distribution in striated muscle. Yet, whether these networks remodel to meet changing mechanical demands or contribute to muscle pathology is unclear. Using C. elegans body-wall muscles, we show that sarcomeres form interconnected networks via actin-, myosin-, and actinin-rich junctions that dynamically remodel in response to locomotor activity. Swimming, which imposes greater mechanical demands, enhances sarcomere branching compared to crawling. In dystrophin-deficient dys-1(eg33) mutants, impaired longitudinal anchorage combined with persistent lateral tension leads to myofibrillar buckling and wavy fiber deformation, echoing features of Duchenne muscular dystrophy. These results position C. elegans as a tractable model for dissecting the biomechanical roles of sarcomere networks in muscle adaptation and disease.