Prmt5 is a regulator of muscle stem cell expansion in adult mice

Ting Zhang, Stefan Günther, Mario Looso, Carsten Künne, Marcus Krüger, Johnny Kim (), Yonggang Zhou () and Thomas Braun ()
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Ting Zhang: Max-Planck Institute for Heart and Lung Research
Stefan Günther: Max-Planck Institute for Heart and Lung Research
Mario Looso: Max-Planck Institute for Heart and Lung Research
Carsten Künne: Max-Planck Institute for Heart and Lung Research
Marcus Krüger: Max-Planck Institute for Heart and Lung Research
Johnny Kim: Max-Planck Institute for Heart and Lung Research
Yonggang Zhou: Max-Planck Institute for Heart and Lung Research
Thomas Braun: Max-Planck Institute for Heart and Lung Research

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: 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.

Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8140

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DOI: 10.1038/ncomms8140

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