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mTOR controls mitochondrial oxidative function through a YY1–PGC-1α transcriptional complex

Author

Listed:
  • John T. Cunningham

    (Harvard Medical School, Boston, Massachusetts 02115, USA
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA)

  • Joseph T. Rodgers

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Daniel H. Arlow

    (Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA and Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02139, USA)

  • Francisca Vazquez

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Vamsi K. Mootha

    (Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA and Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02139, USA)

  • Pere Puigserver

    (Harvard Medical School, Boston, Massachusetts 02115, USA
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA)

Abstract

Mitochondrial sensor The nutrient sensor molecule mTOR (mammalian target of rapamycin) is a kinase involved in the regulation of cell growth and proliferation. Its close links to the cell's energetics suggest that it might interact with the mitochondria, and a computational genomics study now confirms that it does. mTOR balances energy metabolism via transcriptional control of mitochondrial gene expression and oxidative function, with the transcriptional regulators PGC-1a and YY1 as mediators. This pathway opens new possibilities for therapeutic interventions in metabolic diseases in which mitochondrial activity is compromised.

Suggested Citation

  • John T. Cunningham & Joseph T. Rodgers & Daniel H. Arlow & Francisca Vazquez & Vamsi K. Mootha & Pere Puigserver, 2007. "mTOR controls mitochondrial oxidative function through a YY1–PGC-1α transcriptional complex," Nature, Nature, vol. 450(7170), pages 736-740, November.
    • Handle: RePEc:nat:nature:v:450:y:2007:i:7170:d:10.1038_nature06322
    DOI: 10.1038/nature06322
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    Cited by:

    1. Hailiang Zhang & Lin Bai & Xin-Qiang Wu & Xi Tian & Jinwen Feng & Xiaohui Wu & Guo-Hai Shi & Xiaoru Pei & Jiacheng Lyu & Guojian Yang & Yang Liu & Wenhao Xu & Aihetaimujiang Anwaier & Yu Zhu & Da-Long, 2023. "Proteogenomics of clear cell renal cell carcinoma response to tyrosine kinase inhibitor," Nature Communications, Nature, vol. 14(1), pages 1-21, December.
    2. Tomas Venit & Oscar Sapkota & Wael Said Abdrabou & Palanikumar Loganathan & Renu Pasricha & Syed Raza Mahmood & Nadine Hosny El Said & Shimaa Sherif & Sneha Thomas & Salah Abdelrazig & Shady Amin & Da, 2023. "Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice," Nature Communications, Nature, vol. 14(1), pages 1-24, December.

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