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Lsd1 regulates skeletal muscle regeneration and directs the fate of satellite cells

Author

Listed:
  • Milica Tosic

    (Albert-Ludwigs-University Freiburg)

  • Anita Allen

    (Albert-Ludwigs-University Freiburg)

  • Dominica Willmann

    (Albert-Ludwigs-University Freiburg)

  • Christoph Lepper

    (Carnegie Institution)

  • Johnny Kim

    (Max Planck Institute for Heart and Lung Research)

  • Delphine Duteil

    (Albert-Ludwigs-University Freiburg)

  • Roland Schüle

    (Albert-Ludwigs-University Freiburg
    Albert-Ludwigs-University
    Deutsches Konsortium für Translationale Krebsforschung (DKTK)
    K-metics GmbH)

Abstract

Satellite cells are muscle stem cells required for muscle regeneration upon damage. Of note, satellite cells are bipotent and have the capacity to differentiate not only into skeletal myocytes, but also into brown adipocytes. Epigenetic mechanisms regulating fate decision and differentiation of satellite cells during muscle regeneration are not yet fully understood. Here, we show that elevated levels of lysine-specific demethylase 1 (Kdm1a, also known as Lsd1) have a beneficial effect on muscle regeneration and recovery after injury, since Lsd1 directly regulates key myogenic transcription factor genes. Importantly, selective Lsd1 ablation or inhibition in Pax7-positive satellite cells, not only delays muscle regeneration, but changes cell fate towards brown adipocytes. Lsd1 prevents brown adipocyte differentiation of satellite cells by repressing expression of the novel pro-adipogenic transcription factor Glis1. Together, downregulation of Glis1 and upregulation of the muscle-specific transcription program ensure physiological muscle regeneration.

Suggested Citation

  • Milica Tosic & Anita Allen & Dominica Willmann & Christoph Lepper & Johnny Kim & Delphine Duteil & Roland Schüle, 2018. "Lsd1 regulates skeletal muscle regeneration and directs the fate of satellite cells," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02740-5
    DOI: 10.1038/s41467-017-02740-5
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    Cited by:

    1. Qingshuang Cai & Rajesh Sahu & Vanessa Ueberschlag-Pitiot & Sirine Souali-Crespo & Céline Charvet & Ilyes Silem & Félicie Cottard & Tao Ye & Fatima Taleb & Eric Metzger & Roland Schuele & Isabelle M. , 2024. "LSD1 inhibition circumvents glucocorticoid-induced muscle wasting of male mice," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
    2. Ramachandran Prakasam & Angela Bonadiman & Roberta Andreotti & Emanuela Zuccaro & Davide Dalfovo & Caterina Marchioretti & Debasmita Tripathy & Gianluca Petris & Eric N. Anderson & Alice Migazzi & Lau, 2023. "LSD1/PRMT6-targeting gene therapy to attenuate androgen receptor toxic gain-of-function ameliorates spinobulbar muscular atrophy phenotypes in flies and mice," Nature Communications, Nature, vol. 14(1), pages 1-22, December.

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