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Updated: Jan 27, 2026

Minimally Invasive Muscle Embedding MIME - A Novel Experimental Technique to Facilitate Donor-Cell-Mediated Myogenesis
Published on: August 24, 2017
mTOR controls embryonic and adult myogenesis via mTORC1
Nathalie Rion1, Perrine Castets1, Shuo Lin1
1Biozentrum, University of Basel, CH-4056 Basel, Switzerland.
Abstract:
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.This article has an associated 'The people behind the papers' interview.
Insights
The mechanistic target of rapamycin complex 1 (mTORC1) is crucial for muscle stem cell proliferation and fusion during development and regeneration. Its absence leads to perinatal death and impaired muscle repair, highlighting mTORC1
Area of Science:
- Cell Biology
- Developmental Biology
- Muscle Regeneration
Background:
- Muscle fiber formation requires coordinated regulation of progenitor cell proliferation, differentiation, and fusion.
- Intracellular signal coordination during myogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of the cell-growth regulator mTOR, specifically mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2), in mouse muscle progenitor cells.
- To elucidate the function of mTORC1 and mTORC2 in embryonic and adult myogenesis.
Main Methods:
- Elimination of essential components of mTORC1 and mTORC2 in mouse muscle progenitors.
- Analysis of developmental and injury-induced muscle regeneration phenotypes.
Main Results:
- Inactivation of mTORC1, but not mTORC2, in developing muscle leads to perinatal death.
- mTORC1 deficiency in adult muscle stem cells severely impairs injury-induced muscle regeneration.
- Defects in proliferation and fusion capacity of muscle progenitors were observed in mTORC1-deficient cells.
- mTORC1-deficient muscle progenitors retained partial myogenic function.
Conclusions:
- mTORC1, not mTORC2, is a critical regulator of both embryonic and adult myogenesis.
- The study identifies mTORC1 as a key factor in muscle development and repair.
- Alternative pathways may partially compensate for the loss of mTORC1 function.
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