Transcriptional complexes that contain peroxisome-proliferator-activated 
receptor coactivator (PGC)-1alpha control mitochondrial oxidative function to 
maintain energy homeostasis in response to nutrient and hormonal signals. An 
important component in the energy and nutrient pathways is mammalian target of 
rapamycin (mTOR), a kinase that regulates cell growth, size and survival. 
However, it is unknown whether and how mTOR controls mitochondrial oxidative 
activities. Here we show that mTOR is necessary for the maintenance of 
mitochondrial oxidative function. In skeletal muscle tissues and cells, the mTOR 
inhibitor rapamycin decreased the gene expression of the mitochondrial 
transcriptional regulators PGC-1alpha, oestrogen-related receptor alpha and 
nuclear respiratory factors, resulting in a decrease in mitochondrial gene 
expression and oxygen consumption. Using computational genomics, we identified 
the transcription factor yin-yang 1 (YY1) as a common target of mTOR and 
PGC-1alpha. Knockdown of YY1 caused a significant decrease in mitochondrial gene 
expression and in respiration, and YY1 was required for rapamycin-dependent 
repression of those genes. Moreover, mTOR and raptor interacted with YY1, and 
inhibition of mTOR resulted in a failure of YY1 to interact with and be 
coactivated by PGC-1alpha. We have therefore identified a mechanism by which a 
nutrient sensor (mTOR) balances energy metabolism by means of the 
transcriptional control of mitochondrial oxidative function. These results have 
important implications for our understanding of how these pathways might be 
altered in metabolic diseases and cancer.