Induction and stability of the adult myosin phenotype in striated muscles of dwarf mice after chronic thyroid hormone treatment

It is known that a deficiency in thyroid hormone delays the post‐natal maturation of several mammalian tissues. In striated muscle tissue, hypothyroidism delays or inhibits some of the isoform transitions of myosin heavy chains which would occur during normal development. In this paper, using the mouse mutant dwarf , we demonstrate an influence of thyroid hormone on expression of the myosin phenotype in cardiac and skeletal muscle of dwarf mice. Myosin isoforms were identified by gel electrophoresis of native myosin, localised within muscle cells by indirect immunofluorescence and quantified using an ELISA technique. We show that an adult phenotype can be established in both cardiac and skeletal muscle following a treatment involving multiple injections of thyroxine although cardiac musle responds more rapidly. The skeletal myosin phenotype remains stable until at least five weeks after the last injection. In contrast, the fetal form of cardiac myosin reaccumulates upon cessation of thyroxine treatment. Thus, cardiac and skeletal muscles are not only affected differently by the dwarf mutation but also they respond differently to thyroxine treatment and thyroxine withdrawal.