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

John T. Cunningham, Joseph T. Rodgers, Daniel H. Arlow, Francisca Vazquez, Vamsi K. Mootha () and Pere Puigserver ()
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John T. Cunningham: Harvard Medical School, Boston, Massachusetts 02115, 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

Nature, 2007, vol. 450, issue 7170, 736-740

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.

Date: 2007
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DOI: 10.1038/nature06322

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