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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Ting Zhang & Stefan Günther & Mario Looso & Carsten Künne & Marcus Krüger & Johnny Kim & Yonggang Zhou & Thomas Braun, 2015. "Prmt5 is a regulator of muscle stem cell expansion in adult mice," Nature Communications, Nature, vol. 6(1), pages 1-14, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8140
    DOI: 10.1038/ncomms8140
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    Cited by:

    1. Angelina M. Georgieva & Xinyue Guo & Marek Bartkuhn & Stefan Günther & Carsten Künne & Christian Smolka & Ann Atzberger & Ulrich Gärtner & Kamel Mamchaoui & Eva Bober & Yonggang Zhou & Xuejun Yuan & T, 2022. "Inactivation of Sirt6 ameliorates muscular dystrophy in mdx mice by releasing suppression of utrophin expression," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    2. Yasufumi Katanasaka & Harumi Yabe & Noriyuki Murata & Minori Sobukawa & Yuga Sugiyama & Hikaru Sato & Hiroki Honda & Yoichi Sunagawa & Masafumi Funamoto & Satoshi Shimizu & Kana Shimizu & Toshihide Ha, 2024. "Fibroblast-specific PRMT5 deficiency suppresses cardiac fibrosis and left ventricular dysfunction in male mice," Nature Communications, Nature, vol. 15(1), pages 1-13, December.
    3. Wenshu Zeng & Lu Yue & Kim S. W. Lam & Wenxin Zhang & Wai-Kin So & Erin H. Y. Tse & Tom H. Cheung, 2022. "CPEB1 directs muscle stem cell activation by reprogramming the translational landscape," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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