期刊
DEVELOPMENT
卷 146, 期 7, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.172460
关键词
Raptor; Rictor; Protein synthesis; Satellite cells; Muscle regeneration; Rapamycin
资金
- Canton of Basel-Stadt
- Canton of Basel-Landschaft
- Schweizerischer Nationalfonds zur Forderung der Wissenschaftlichen Forschung
- Biozentrum PhD Fellowship
The formation of multi-nucleated muscle fibers from progenitors requires the fine-tuned and coordinated regulation of proliferation, differentiation and fusion, both during development and after injury in the adult. Although some of the key factors that are involved in the different steps are well known, how intracellular signals are coordinated and integrated is largely unknown. Here, we investigated the role of the cell-growth regulator mTOR by eliminating essential components of the mTOR complexes 1 (mTORC1) and 2 (mTORC2) in mouse muscle progenitors. We show that inactivation of mTORC1, but not mTORC2, in developing muscle causes perinatal death. In the adult, mTORC1 deficiency in muscle stem cells greatly impinges on injury-induced muscle regeneration. These phenotypes are because of defects in the proliferation and fusion capacity of the targeted muscle progenitors. However, mTORC1-deficient muscle progenitors partially retain their myogenic function. Hence, our results show that mTORC1 and not mTORC2 is an important regulator of embryonic and adult myogenesis, and they point to alternative pathways that partially compensate for the loss of mTORC1.
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