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Sci Rep. 2016 Jul 26;6:30027. doi: 10.1038/srep30027.

Mitochondrial Mg(2+) homeostasis decides cellular energy metabolism and vulnerability to stress.

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Center for Biosciences and Informatics, School of Fundamental Science and Technology Graduate School of Science and Technology, Keio University, Yokohama, 223-8522, Kanagawa, Japan.
Institute for Advanced Biosciences, Keio University, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Center for Science and Technology for Designing Functions, School of Integrated Design Engineering, Graduate School of Science and Technology, Keio University, Yokohama, Kanagawa, 223-8522, Japan.


Cellular energy production processes are composed of many Mg(2+) dependent enzymatic reactions. In fact, dysregulation of Mg(2+) homeostasis is involved in various cellular malfunctions and diseases. Recently, mitochondria, energy-producing organelles, have been known as major intracellular Mg(2+) stores. Several biological stimuli alter mitochondrial Mg(2+) concentration by intracellular redistribution. However, in living cells, whether mitochondrial Mg(2+) alteration affect cellular energy metabolism remains unclear. Mg(2+) transporter of mitochondrial inner membrane MRS2 is an essential component of mitochondrial Mg(2+) uptake system. Here, we comprehensively analyzed intracellular Mg(2+) levels and energy metabolism in Mrs2 knockdown (KD) cells using fluorescence imaging and metabolome analysis. Dysregulation of mitochondrial Mg(2+) homeostasis disrupted ATP production via shift of mitochondrial energy metabolism and morphology. Moreover, Mrs2 KD sensitized cellular tolerance against cellular stress. These results indicate regulation of mitochondrial Mg(2+) via MRS2 critically decides cellular energy status and cell vulnerability via regulation of mitochondrial Mg(2+) level in response to physiological stimuli.

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