Myosin is the only one of the many protein components of muscle that has been shown to exhibit differences between fetal and adult forms. The existence of qualitative changes in myosin during development has been shown to be species dependent. Little is known regarding the ontogeny of mouse myosin. The underlying mechanisms for the control of synthesis of fetal and adult myosin have not been elucidated. Furthermore the relationship between these forms in hereditary muscle diseases is not clear. The principal objective of the proposed research is to investigate normal muscle development and hereditary diseases of muscle. This objective will be pursued by the biochemical analysis of myosin during development in inbred mice. In addition, these studies will be aided by an analysis of the fetal and adult myosin in inbred dystrophic and dysgenic strains of mice. Preliminary results in our laboratory have revealed the existence of a putative fetal myosin in mice. We propose to: (1) examine further the structural and functional similarities and differences between the putative fetal and adult myosin by comparing their molecular weights, myosin-like ATPase activities, substructures such as heavy meromyosin and subfragment I, and the 3-methylhistidine content; (2) analyze the transition from fetal myosin synthesis to that of the adult type during development in various muscle tissues; and (3) demonstrate any differences which may exist between myosin from mice with hereditary muscle diseases such as muscular dystrophy and muscular dysgenesis and normal animals. And to further examine if there are any biochemical differences with respect to fetal and adult myosin between mutant and normal mice.