Myogenesis in embryos and regenerating adult muscles requires coordinated proliferation, differentiation and fusion of progenitor cells. The molecular control of this process has been well studied, but many of the key underlying factors remain incompletely understood, as exemplified by the growth regulator mTOR. mTOR is a protein kinase that forms two distinct complexes: mTORC1 (with the essential component raptor) and mTORC2 (with the essential component rictor). While both complexes have been implicated in myogenesis, the chemical inhibition typically used to interrogate them has its drawbacks. Markus Rüegg and colleagues now tackle this problem with genetics, by conditionally ablating Rptor and Rictor. Loss of Rptor in embryonic skeletal muscle progenitors is lethal and impairs the first wave of myogenesis without completely abolishing myofiber formation. Rptor-deleted cells show reduced protein synthesis, reduced proliferation and reduced propensity to fuse in differentiation medium. Rptor deletion in adult quiescent satellite stem cells does not reduce their number; however, regeneration is severely impaired after injury due to deficient proliferation and a delayed activation and commitment to the myogenic lineage. In contrast, Rictor deletion (and hence loss of mTORC2 activity) does not impair embryonic or adult regenerative myogenesis. A key signaling protein thus acts exclusively through one of its complexes – mTORC1 – to regulate muscle development.
mTORC1 manages mouse myogenesis
mTORC1 manages mouse myogenesis. Development 1 April 2019; 146 (7): e0704. doi:
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