Author
Listed:
- Takashi Baba
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Hiroyuki Otake
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Tetsuya Sato
(Medical Institute of Bioregulation, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Kanako Miyabayashi
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Yurina Shishido
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Chia-Yih Wang
(Institute of Molecular Biology, Academia Sinica, 128 Academia Road, Nankang
Present address: Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan)
- Yuichi Shima
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Hiroshi Kimura
(Nuclear Dynamics Group, Graduate School of Frontier Biosciences, Osaka University, Yamadaoka 1-3)
- Mikako Yagi
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Yasuhiro Ishihara
(Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University, Kagamiyama 1-7-1)
- Shinjiro Hino
(Institute of Molecular Embryology and Genetics, Kumamoto University, Honjo 2-2-1, Chuo-ku)
- Hidesato Ogawa
(Nuclear Dynamics Group, Graduate School of Frontier Biosciences, Osaka University, Yamadaoka 1-3
Advanced ICT Research Institute Kobe, National Institute of Information and Communications Technology, Iwaoka 588-2, Nishi-ku)
- Mitsuyoshi Nakao
(Institute of Molecular Embryology and Genetics, Kumamoto University, Honjo 2-2-1, Chuo-ku)
- Takeshi Yamazaki
(Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University, Kagamiyama 1-7-1)
- Dongchon Kang
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Yasuyuki Ohkawa
(JST-CREST, Faculty of Medicine, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Mikita Suyama
(Medical Institute of Bioregulation, Kyushu University, Maidashi 3-1-1, Higashi-ku)
- Bon-Chu Chung
(Institute of Molecular Biology, Academia Sinica, 128 Academia Road, Nankang)
- Ken-Ichirou Morohashi
(Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku)
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 α, the present study raises the possibility that certain types of nuclear receptors regulate sets of genes involved in metabolic pathways to generate energy carriers.
Suggested Citation
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 &, 2014.
"Glycolytic genes are targets of the nuclear receptor Ad4BP/SF-1,"
Nature Communications, Nature, vol. 5(1), pages 1-13, May.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4634
DOI: 10.1038/ncomms4634
Download full text from publisher
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4634. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.