EID-1 Interacts with Orphan Nuclear Receptor SF-1 and Represses Its Transactivation

  • Park, Yun-Yong (Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University) ;
  • Park, Ki Cheol (Laboratory of Endocrine Cell Biology, Department of Internal Medicine, Chungnam National University College of Medicine) ;
  • Shong, Minho (Laboratory of Endocrine Cell Biology, Department of Internal Medicine, Chungnam National University College of Medicine) ;
  • Lee, Soon-Jung (Department of Anatomy, Chungnam National University College of Medicine) ;
  • Lee, Young-Ho (Department of Anatomy, Chungnam National University College of Medicine) ;
  • Choi, Hueng-Sik (Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University)
  • Received : 2007.05.11
  • Accepted : 2007.06.26
  • Published : 2007.12.31

Abstract

The orphan nuclear receptor, SF-1, plays a pivotal role in the development and differentiation of the endocrine and reproductive systems, and also regulates the transcription of a host of genes, including those encoding several steroidogenic enzymes and gonadotropins. We found that a previously unidentified repressor, EID-1, is an SF-1-interacting protein that inhibits the transactivation of SF-1. A transient transfection assay revealed that EID-1 inhibits SF-1, but not LRH-1, $ERR{\gamma}$, or mCAR. Using the yeast two hybrid and GST pull-down assays, we determined that EID-1 interacted strongly with SF-1. In addition, it colocalized with SF-1 in mammalian cells and interacted specifically with the AF-2 domain of SF-1, competing with SRC-1 to inhibit SF-1 transactivation. EID-1 is expressed in the mouse testis, and its expression decreases during testis development. The results of the present study suggest that EID-1 can act as a repressor, regulating the function of SF-1.

Keywords

Acknowledgement

Supported by : National Research Laboratory

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