Characterization of muscle growth and sarcomere branching in the striated musculature ofC. elegans

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. Significance Statement Sarcomere networks interconnect contractile fibers and are thought to distribute forces laterally across muscles. However, whether these networks dynamically remodel to meet mechanical demands or contribute to disease remains unknown. Here, we show that sarcomere networks in C. elegans body-wall muscles display activity-dependent plasticity and incorporate force-generating components. In dystrophin-deficient mutants, the persistence of lateral tension, combined with impaired longitudinal anchorage, correlates with myofibrillar buckling and wavy fiber deformation. These findings suggest that sarcomere networks are dynamic mechanical structures that adapt to contractile demands and influence muscle integrity during disease