Transcription profiling of mouse TSC2-/- embryonic fibroblasts: vehicle-treated, rapamycin-treated, gfp-infected, and pgc-1alpha-infected samples reveals the mTOR pathway controls mitochondrial gene expression and respiration through the YY1/PGC-1alpha transcriptional complex

ABSTRACT: Mitochondrial oxidative function is tightly controlled to maintain energy homeostasis in response to nutrient and hormonal signals. An important cellular component in the energy sensing response is the target of rapamycin (TOR) kinase pathway; however whether and how mTOR controls mitochondrial oxidative activity is unknown. Here, we show that mTOR kinase activity stimulates mitochondrial gene expression and oxidative function. In skeletal muscle cells and TSC2-/- MEFs, the mTOR inhibitor rapamycin largely decreased gene expression of mitochondrial transcriptional regulators such as PGC-1alpha and the transcription factors ERRalpha and NRFs. As a consequence, mitochondrial gene expression and oxygen consumption were reduced upon mTOR inhibition. Using computational genomics, we identified

ORGANISM(S): Mus musculus

SUBMITTER: Pere Puigserver 

PROVIDER: E-GEOD-5332 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress