Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1

Takashi Baba; Hiroyuki Otake; Tetsuya Sato; Kanako Miyabayashi; Yurina Shishido; Chia Yih Wang; Yuichi Shima; Hiroshi Kimura; Mikako Yagi; Yasuhiro Ishihara; Shinjiro Hino; Hidesato Ogawa; Mitsuyoshi Nakao; Takeshi Yamazaki; Dongchon Kang; Yasuyuki Ohkawa; Mikita Suyama; Bon Chu Chung; Ken Ichirou Morohashi

doi:10.1038/ncomms4634

Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1

Takashi Baba, Hiroyuki Otake, Tetsuya Sato, Kanako Miyabayashi, Yurina Shishido, Chia Yih Wang, Yuichi Shima, Hiroshi Kimura, Mikako Yagi, Yasuhiro Ishihara, Shinjiro Hino, Hidesato Ogawa, Mitsuyoshi Nakao, Takeshi Yamazaki, Dongchon Kang, Yasuyuki Ohkawa, Mikita Suyama, Bon Chu Chung, Ken Ichirou Morohashi

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Abstract

Genetic deficiencies in transcription factors can lead to the loss of certain types of cells and tissue. The steroidogenic tissue-specific nuclear receptor Ad4BP/SF-1 (NR5A1) is one such gene, because mice in which this gene is disrupted fail to develop the adrenal gland and gonads. However, the specific role of Ad4BP/SF-1 in these biological events remains unclear. Here we use chromatin immunoprecipitation sequencing to show that nearly all genes in the glycolytic pathway are regulated by Ad4BP/SF-1. Suppression of Ad4BP/SF-1 by small interfering RNA reduces production of the energy carriers ATP and nicotinamide adenine dinucleotide phosphate, as well as lowers expression of genes involved in glucose metabolism. Together, these observations may explain tissue dysgenesis as a result of Ad4BP/SF-1 gene disruption in vivo. Considering the function of estrogen-related receptor Î±, the present study raises the possibility that certain types of nuclear receptors regulate sets of genes involved in metabolic pathways to generate energy carriers.

Original language	English
Article number	3634
Journal	Nature communications
Volume	5
DOIs	https://doi.org/10.1038/ncomms4634
Publication status	Published - Apr 14 2014

All Science Journal Classification (ASJC) codes

General Chemistry
General Biochemistry,Genetics and Molecular Biology
General Physics and Astronomy

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Baba, T., Otake, H., Sato, T., Miyabayashi, K., Shishido, Y., Wang, C. Y., Shima, Y., Kimura, H., Yagi, M., Ishihara, Y., Hino, S., Ogawa, H., Nakao, M., Yamazaki, T., Kang, D., Ohkawa, Y., Suyama, M., Chung, B. C., & Morohashi, K. I. (2014). Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1. Nature communications, 5, Article 3634. https://doi.org/10.1038/ncomms4634

@article{aacd58d3110d4cbe8efffe35bff3357a,

title = "Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1",

abstract = "Genetic deficiencies in transcription factors can lead to the loss of certain types of cells and tissue. The steroidogenic tissue-specific nuclear receptor Ad4BP/SF-1 (NR5A1) is one such gene, because mice in which this gene is disrupted fail to develop the adrenal gland and gonads. However, the specific role of Ad4BP/SF-1 in these biological events remains unclear. Here we use chromatin immunoprecipitation sequencing to show that nearly all genes in the glycolytic pathway are regulated by Ad4BP/SF-1. Suppression of Ad4BP/SF-1 by small interfering RNA reduces production of the energy carriers ATP and nicotinamide adenine dinucleotide phosphate, as well as lowers expression of genes involved in glucose metabolism. Together, these observations may explain tissue dysgenesis as a result of Ad4BP/SF-1 gene disruption in vivo. Considering the function of estrogen-related receptor {\^I}±, the present study raises the possibility that certain types of nuclear receptors regulate sets of genes involved in metabolic pathways to generate energy carriers.",

author = "Takashi Baba and Hiroyuki Otake and Tetsuya Sato and Kanako Miyabayashi and Yurina Shishido and Wang, {Chia Yih} and Yuichi Shima and Hiroshi Kimura and Mikako Yagi and Yasuhiro Ishihara and Shinjiro Hino and Hidesato Ogawa and Mitsuyoshi Nakao and Takeshi Yamazaki and Dongchon Kang and Yasuyuki Ohkawa and Mikita Suyama and Chung, {Bon Chu} and Morohashi, {Ken Ichirou}",

note = "Funding Information: This work was supported by Grants 21249018 (K.M.) and 10007695 (T.B.) from the Japan Society for the Promotion of Science (JSPS); Grant 22132002 (K.M.) from the Ministry of Education, Culture, Sports, Science, and Technology, Japan (MEXT) KAKENHI; the Tokyo Biochemical Research Foundation (K.M.); Kyushu University Interdisciplinary Program in Education and Projects in Research Development (T.B.); the Fukuoka Foundation for Sound Health (T.B.); and Grant NSC-101-2321-B-001-001 (B.-C.C.) from the National Science Council, Taiwan. We thank Dr Megumi Tsuchiya and Ms Junko Nagai for technical assistance.",

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doi = "10.1038/ncomms4634",

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T1 - Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1

AU - Baba, Takashi

AU - Otake, Hiroyuki

AU - Sato, Tetsuya

AU - Miyabayashi, Kanako

AU - Shishido, Yurina

AU - Wang, Chia Yih

AU - Shima, Yuichi

AU - Kimura, Hiroshi

AU - Yagi, Mikako

AU - Ishihara, Yasuhiro

AU - Hino, Shinjiro

AU - Ogawa, Hidesato

AU - Nakao, Mitsuyoshi

AU - Yamazaki, Takeshi

AU - Kang, Dongchon

AU - Ohkawa, Yasuyuki

AU - Suyama, Mikita

AU - Chung, Bon Chu

AU - Morohashi, Ken Ichirou

N1 - Funding Information: This work was supported by Grants 21249018 (K.M.) and 10007695 (T.B.) from the Japan Society for the Promotion of Science (JSPS); Grant 22132002 (K.M.) from the Ministry of Education, Culture, Sports, Science, and Technology, Japan (MEXT) KAKENHI; the Tokyo Biochemical Research Foundation (K.M.); Kyushu University Interdisciplinary Program in Education and Projects in Research Development (T.B.); the Fukuoka Foundation for Sound Health (T.B.); and Grant NSC-101-2321-B-001-001 (B.-C.C.) from the National Science Council, Taiwan. We thank Dr Megumi Tsuchiya and Ms Junko Nagai for technical assistance.

PY - 2014/4/14

Y1 - 2014/4/14

N2 - Genetic deficiencies in transcription factors can lead to the loss of certain types of cells and tissue. The steroidogenic tissue-specific nuclear receptor Ad4BP/SF-1 (NR5A1) is one such gene, because mice in which this gene is disrupted fail to develop the adrenal gland and gonads. However, the specific role of Ad4BP/SF-1 in these biological events remains unclear. Here we use chromatin immunoprecipitation sequencing to show that nearly all genes in the glycolytic pathway are regulated by Ad4BP/SF-1. Suppression of Ad4BP/SF-1 by small interfering RNA reduces production of the energy carriers ATP and nicotinamide adenine dinucleotide phosphate, as well as lowers expression of genes involved in glucose metabolism. Together, these observations may explain tissue dysgenesis as a result of Ad4BP/SF-1 gene disruption in vivo. Considering the function of estrogen-related receptor Î±, the present study raises the possibility that certain types of nuclear receptors regulate sets of genes involved in metabolic pathways to generate energy carriers.

AB - Genetic deficiencies in transcription factors can lead to the loss of certain types of cells and tissue. The steroidogenic tissue-specific nuclear receptor Ad4BP/SF-1 (NR5A1) is one such gene, because mice in which this gene is disrupted fail to develop the adrenal gland and gonads. However, the specific role of Ad4BP/SF-1 in these biological events remains unclear. Here we use chromatin immunoprecipitation sequencing to show that nearly all genes in the glycolytic pathway are regulated by Ad4BP/SF-1. Suppression of Ad4BP/SF-1 by small interfering RNA reduces production of the energy carriers ATP and nicotinamide adenine dinucleotide phosphate, as well as lowers expression of genes involved in glucose metabolism. Together, these observations may explain tissue dysgenesis as a result of Ad4BP/SF-1 gene disruption in vivo. Considering the function of estrogen-related receptor Î±, the present study raises the possibility that certain types of nuclear receptors regulate sets of genes involved in metabolic pathways to generate energy carriers.

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VL - 5

JO - Nature communications

JF - Nature communications

M1 - 3634

ER -

Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1

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