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p107 mediated mitochondrial function controls muscle stem cell proliferative fates

Author

Listed:
  • Debasmita Bhattacharya

    (York University
    York University)

  • Vicky Shah

    (York University
    York University)

  • Oreoluwa Oresajo

    (York University
    York University)

  • Anthony Scimè

    (York University
    York University
    York University)

Abstract

Muscle diseases and aging are associated with impaired myogenic stem cell self-renewal and fewer proliferating progenitors (MPs). Importantly, distinct metabolic states induced by glycolysis or oxidative phosphorylation have been connected to MP proliferation and differentiation. However, how these energy-provisioning mechanisms cooperate remain obscure. Herein, we describe a mechanism by which mitochondrial-localized transcriptional co-repressor p107 regulates MP proliferation. We show p107 directly interacts with the mitochondrial DNA, repressing mitochondrial-encoded gene transcription. This reduces ATP production by limiting electron transport chain complex formation. ATP output, controlled by the mitochondrial function of p107, is directly associated with the cell cycle rate. Sirt1 activity, dependent on the cytoplasmic glycolysis product NAD+, directly interacts with p107, impeding its mitochondrial localization. The metabolic control of MP proliferation, driven by p107 mitochondrial function, establishes a cell cycle paradigm that might extend to other dividing cell types.

Suggested Citation

  • Debasmita Bhattacharya & Vicky Shah & Oreoluwa Oresajo & Anthony Scimè, 2021. "p107 mediated mitochondrial function controls muscle stem cell proliferative fates," Nature Communications, Nature, vol. 12(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-26176-0
    DOI: 10.1038/s41467-021-26176-0
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    References listed on IDEAS

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