The basement membrane of skeletal muscle, which is composed of extracellular matrix (ECM) molecules such as laminin, plays an important role not only in maintaining the physical strength of muscle tissue but also in the unique tissue plasticity of skeletal muscle, such as responses to mechanical environments, i.e. exercise and immobility (hypertrophy/atrophy), and myogenesis/regeneration. An interface between the ECM and cells is essential to transmit ECM information, which dynamically and spatiotemporally changes in response to the environment, to muscle cells and to appropriately activate cellular responses involved in plasticity. Dystroglycan (DG) is a major matrix receptor, that is an interface molecule, in skeletal muscle, and while it plays an important role in the formation and regeneration of muscle tissue, its reduced matrix binding ability can cause diseases such as muscular dystrophy. However, it is still unclear how ECM information is transmitted to muscle cells via DG and what kind of signals are involved in the regulation of plasticity. In this study, we will elucidate DG-dependent ECM signaling pathways and their significance in response to mechanical environments and in myogenesis and regeneration using various mouse models that lack or enhance the ECM-binding ability of DG. The molecular mechanisms of ECM signaling that regulate skeletal muscle plasticity will be elucidated, and the findings obtained will be used to elucidate the pathophysiology of muscle diseases and to develop therapeutic strategies.