Myostatin is a key negative regulator of skeletal muscle mass development in vertebrates. Recent studies have vastly expanded our understanding of the cellular and molecular mechanisms by which Myostatin acts to regulate the size of skeletal muscle within the vertebrate body. In order to understand the origins of skeletal muscle size increases, it is vital to gain a full understanding of the role that Myostatin plays during prenatal life. This review brings together data from numerous animal models to establish the mechanisms of Myostatin action during embryonic and foetal development. We highlight the temporal and spatial control of Myostatin expression in a variety of vertebrate species and the mechanisms by which Myostatin gene expression is regulated. We draw attention to the key loss- and gain-of-function developmental experiments to formulate a model to explain how Myostatin acts to control skeletal muscle growth during development.
Keywords: Myostatin, development, myogenesis, skeletal, muscle, expression, stem, cell, vertebrates, GDF8, BMPs, GDFs, Inhibins, ALK-4, Smad2/3/4, MEF2C, MyoD, cyclin kinase, PI3K, AKT/PKB, phenotype, Epinephelus coioides, Lates calcarifer, Oncorhynchus mykiss, Salvelinus fontinalis, Danio rerio, TMyostatin1, tMyostatin2, zfMSTN-1, zfMSTN-2, Wnts, ectoderm, Follistatin, Pax7, wild type, genetic ablation, Act IIA/B, Danio rario, Gallus gallus, Mus musculis, hypotrophic, myofibre, adipocyte, C1QTNF3, HMGA2, Myogenin, asRNA, dystrophin, dystroglycan, sarcoglycan, myotome, MHC, transcription, progenitor cell
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