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In this study, we show that muscle-specific inactivation of mTOR leads to severe myopathy, resulting in premature death. mTOR-deficient muscles display metabolic changes similar to those observed in muscles lacking raptor, including impaired oxidative metabolism, altered mitochondrial regulation, and glycogen accumulation associated with protein kinase B\/Akt hyperactivation. In addition, mTOR-deficient muscles exhibit increased basal glucose uptake, whereas whole body glucose homeostasis is essentially maintained. Importantly, loss of mTOR exacerbates the myopathic features in both slow oxidative and fast glycolytic muscles. Moreover, mTOR but not raptor and rictor deficiency leads to reduced muscle dystrophin content. We provide evidence that mTOR controls dystrophin transcription in a cell-autonomous, rapamycin-resistant, and kinase-independent manner. Collectively, our results demonstrate that mTOR acts mainly via mTORC1, whereas regulation of dystrophin is raptor and rictor independent.<\/jats:p>","DOI":"10.1083\/jcb.200903131","type":"journal-article","created":{"date-parts":[[2009,12,14]],"date-time":"2009-12-14T18:28:35Z","timestamp":1260815315000},"page":"859-874","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":363,"title":["Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy"],"prefix":"10.1083","volume":"187","author":[{"given":"Val\u00e9rie","family":"Risson","sequence":"first","affiliation":[{"name":"Laboratoire de Biologie Mol\u00e9culaire de la Cellule, Centre National de la Recherche Scientifique, Unit\u00e9 Mixte de Recherche 5239, IFR128, Universit\u00e9 de Lyon, Equipe Diff\u00e9renciation Neuromusculaire, Ecole Normale Sup\u00e9rieure, 69364 Lyon Cedex 07, France 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