Elevated rates of force development and MgATP binding in F764L and S532P myosin mutations causing dilated cardiomyopathy

► F764L and S532P point mutations were engineered into mouse cardiac myosin. ► Dilated cardiomyopathy developed in heterozygous F764L/+ and S532P/+ mice. ► Myocardial strips exhibited higher rates of force development and MgATP binding. ► These alterations in myofilament function preceded development of DCM.