Prmt5 is a regulator of muscle stem cell expansion in adult mice
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Updated: Apr 11, 2026
Author Spotlight: Ex Vivo Protocol for Culturing Quiescent Muscle Stem Cells with Niche Components
Published on: June 2, 2023
Ting Zhang1, Stefan Günther1, Mario Looso1
1Department of Cardiac Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.
Abstract:
Skeletal muscle stem cells (MuSC), also called satellite cells, are indispensable for maintenance and regeneration of adult skeletal muscles. Yet, a comprehensive picture of the regulatory events controlling the fate of MuSC is missing. Here, we determine the proteome of MuSC to design a loss-of-function screen, and identify 120 genes important for MuSC function including the arginine methyltransferase Prmt5. MuSC-specific inactivation of Prmt5 in adult mice prevents expansion of MuSC, abolishes long-term MuSC maintenance and abrogates skeletal muscle regeneration. Interestingly, Prmt5 is dispensable for proliferation and differentiation of Pax7(+) myogenic progenitor cells during mouse embryonic development, indicating significant differences between embryonic and adult myogenesis. Mechanistic studies reveal that Prmt5 controls proliferation of adult MuSC by direct epigenetic silencing of the cell cycle inhibitor p21. We reason that Prmt5 generates a poised state that keeps MuSC in a standby mode, thus allowing rapid MuSC amplification under disease conditions.
Insights
Arginine methyltransferase Prmt5 is crucial for adult skeletal muscle stem cell (MuSC) function and regeneration. Prmt5 maintains MuSC by epigenetically silencing the p21 cell cycle inhibitor, ensuring readiness for repair.
Area of Science:
- Cell Biology
- Developmental Biology
- Muscle Physiology
Background:
- Skeletal muscle stem cells (MuSCs), or satellite cells, are vital for adult muscle maintenance and repair.
- The regulatory mechanisms governing MuSC fate and function remain incompletely understood.
Purpose of the Study:
- To identify key genes regulating adult MuSC function through a proteomic and loss-of-function screen.
- To elucidate the specific role of arginine methyltransferase Prmt5 in adult myogenesis and skeletal muscle regeneration.
Main Methods:
- Proteomic analysis of MuSCs.
- Development of a MuSC-specific loss-of-function screen in adult mice.
- Mechanistic studies investigating Prmt5's role in cell cycle regulation.
Main Results:
- Identified 120 genes critical for MuSC function, including Prmt5.
- MuSC-specific Prmt5 inactivation in adult mice impaired MuSC expansion, long-term maintenance, and muscle regeneration.
- Prmt5 was found to be dispensable for embryonic myogenesis.
- Prmt5 epigenetically silences p21, a cell cycle inhibitor, to control adult MuSC proliferation.
Conclusions:
- Prmt5 plays a critical role in adult skeletal muscle stem cell proliferation and maintenance.
- Prmt5-mediated epigenetic regulation of p21 is essential for keeping adult MuSCs in a poised state for rapid response to injury.
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