FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure

Shinjiro Hino (), Akihisa Sakamoto, Katsuya Nagaoka, Kotaro Anan, Yuqing Wang, Shinya Mimasu, Takashi Umehara, Shigeyuki Yokoyama, Ken-ichiro Kosai and Mitsuyoshi Nakao ()
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Shinjiro Hino: Institute of Molecular Embryology and Genetics, the Global Center of Excellence 'Cell Fate Regulation Research and Education Unit', Kumamoto University
Akihisa Sakamoto: Institute of Molecular Embryology and Genetics, the Global Center of Excellence 'Cell Fate Regulation Research and Education Unit', Kumamoto University
Katsuya Nagaoka: Institute of Molecular Embryology and Genetics, the Global Center of Excellence 'Cell Fate Regulation Research and Education Unit', Kumamoto University
Kotaro Anan: Institute of Molecular Embryology and Genetics, the Global Center of Excellence 'Cell Fate Regulation Research and Education Unit', Kumamoto University
Yuqing Wang: Advanced Therapeutics Course, Graduate School of Medical and Dental Sciences, Kagoshima University
Shinya Mimasu: RIKEN Systems and Structural Biology Center
Takashi Umehara: RIKEN Systems and Structural Biology Center
Shigeyuki Yokoyama: RIKEN Systems and Structural Biology Center
Ken-ichiro Kosai: Advanced Therapeutics Course, Graduate School of Medical and Dental Sciences, Kagoshima University
Mitsuyoshi Nakao: Institute of Molecular Embryology and Genetics, the Global Center of Excellence 'Cell Fate Regulation Research and Education Unit', Kumamoto University

Nature Communications, 2012, vol. 3, issue 1, 1-12

Abstract: Abstract Environmental factors such as nutritional state may act on the epigenome that consequently contributes to the metabolic adaptation of cells and the organisms. The lysine-specific demethylase-1 (LSD1) is a unique nuclear protein that utilizes flavin adenosine dinucleotide (FAD) as a cofactor. Here we show that LSD1 epigenetically regulates energy-expenditure genes in adipocytes depending on the cellular FAD availability. We find that the loss of LSD1 function, either by short interfering RNA or by selective inhibitors in adipocytes, induces a number of regulators of energy expenditure and mitochondrial metabolism such as PPARγ coactivator-1α resulting in the activation of mitochondrial respiration. In the adipose tissues from mice on a high-fat diet, expression of LSD1-target genes is reduced, compared with that in tissues from mice on a normal diet, which can be reverted by suppressing LSD1 function. Our data suggest a novel mechanism where LSD1 regulates cellular energy balance through coupling with cellular FAD biosynthesis.

Date: 2012
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DOI: 10.1038/ncomms1755

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