期刊
CELL METABOLISM
卷 18, 期 5, 页码 698-711出版社
CELL PRESS
DOI: 10.1016/j.cmet.2013.10.001
关键词
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资金
- Terry Fox Research Institute [TFF-116128]
- Canadian Institutes of Health Research [CIHR MOP-7214, MOP-115195, MOP-106603]
- Canadian Cancer Society Research Institute [CCSRI 16208]
- CIHR
- Canadian Diabetes Association
- Canderel fellowship
- Canada Foundation of Innovation
- Dr. John R. and Clara M. Fraser Memorial Trust
- Terry Fox Foundation
- Canadian Institutes of Health Research
- McGill University
- Natural Sciences and Engineering Research Council of Canada
- Canada Foundation for Innovation
- Quebec ministere de la recherche en science et technologie
mRNA translation is thought to be the most energy-consuming process in the cell. Translation and energy metabolism are dysregulated in a variety of diseases including cancer, diabetes, and heart disease. However, the mechanisms that coordinate translation and energy metabolism in mammals remain largely unknown. The mechanistic/mammalian target of rapamycin complex 1 (mTORC1) stimulates mRNA translation and other anabolic processes. We demonstrate that mTORC1 controls mitochondrial activity and biogenesis by selectively promoting translation of nucleus-encoded mitochondria-related mRNAs via inhibition of the eukaryotic translation initiation factor 4E (eIF4E)-binding proteins (4E-BPs). Stimulating the translation of nucleus-encoded mitochondria-related mRNAs engenders an increase in ATP production capacity, a required energy source for translation. These findings establish a feed-forward loop that links mRNA translation to oxidative phosphorylation, thereby providing a key mechanism linking aberrant mTOR signaling to conditions of abnormal cellular energy metabolism such as neoplasia and insulin resistance.
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