The protein, dysferlin, mediates sarcolemmal repair in vitro, implicating defective membrane
repair in dysferlinopathies. To study the role of dysferlin in vivo, we assessed contractile
function, sarcolemmal integrity, and myogenesis before and after injury from large-strain
lengthening contractions in dysferlin-null and control mice. We report that dysferlin-null
muscles produce higher contractile torque, and are equally susceptible to initial injury but
recover from injury more slowly. Two weeks after injury, control muscles retain fluorescein …