title: Myosin expression in hypertrophied fast twitch and slow tonic muscles of normal and dystrophic chickens.
abstract: Disruption of the development program of myosin gene expression has been reported in chicken muscular dystrophy. In the present report, the relationship between muscular dystrophy and the ability of muscle to respond to an increased work load with a transition in the myosin phenotype has been investigated. Hypertrophy of slow tonic anterior latissimus dorsi (ALD) and fast twitch patagialis (PAT) muscles was induced by overloading for 35 days and myosin expression was analyzed by electrophoresis and immunocytochemistry. Normal and dystrophic chicken ALD muscles have nearly identical proportions of SM-1 and SM-2 isomyosins and both exhibit an age-related repression of the SM-1 isomyosin which is enhanced and accelerated by overloading. Immunocytochemistry with anti-myosin heavy chain (MHC) antibodies demonstrates the appearance of nascent myofibers in overloaded ALD muscles from both normal and dystrophic chickens. A minor fast twitch fiber population is also identified which doubles in number with overloading in normal ALD muscles. There are only half as many fast twitch fibers in control dystrophic ALD muscles and this number does not increase with overloading. In contrast to ALD muscles, the isomyosin profile of normal and dystrophic PAT muscles is quite different. There is significantly more FM-3 and significantly less FM-1 isomyosin in the dystrophic PAT muscle. However, both normal and dystrophic PAT muscles exhibit an overload-induced accumulation of the FM-3 isomyosin. Immunocytochemistry reveals that, unlike the normal PAT muscle, the dystrophic PAT muscle contains a population of myofibers which express slow MHCs. As in the ALD muscle, overload-induced hypertrophy is associated with a repression of the SM-1 MHC in these fibers. Nascent myofiber formation does not occur in either normal or dystrophic overloaded PAT muscles.
authors.affiliation: Department of Physiology and Biophysics, University of Illinois, Chicago 60680.
authors.forename: J M
authors.initials: JM
authors.lastname: Kennedy
authors.forename: R
authors.initials: R
authors.lastname: Zak
authors.forename: L
authors.initials: L
authors.lastname: Gao
mesh_terms: D000818:Animals; D001284:Atrophy; D002645:Chickens; D003238:Connective Tissue / Q000473:pathology; D004586:Electrophoresis; D006984:Hypertrophy; D007150:Immunohistochemistry; D009132:Muscles / Q000737:chemistry* / Q000473:pathology; D009137:Muscular Dystrophy, Animal / Q000378:metabolism* / Q000473:pathology; D009210:Myofibrils / Q000737:chemistry / Q000648:ultrastructure; D015879:Myosin Subfragments / Q000032:analysis / Q000145:classification; D009218:Myosins / Q000032:analysis* / Q000145:classification
chemical_list: D015879:Myosin Subfragments; D009218:Myosins