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EID‐1 interacts with the orphan nuclear receptor SF‐1 and represses its transactivation
Author(s) -
Kim DonKyu,
Park YunYong,
Choi HuengSik
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.782.22
Subject(s) - transactivation , repressor , neuron derived orphan receptor 1 , nuclear receptor , corepressor , transcription factor , microbiology and biotechnology , biology , transcription (linguistics) , gene , steroidogenic factor 1 , chemistry , genetics , linguistics , philosophy
The orphan nuclear receptor, SF‐1, plays a pivotal role on the development and differentiation of the endocrine and reproductive systems, and also regulates the transcription of a host of genes, including several steroidogenic enzymes and gonadotropin genes. Here, we demonstrate that a previously unidentified repressor, EID‐1, is a novel SF‐1 interacting protein, which represses the transactivation of SF‐1. A transient transfection assay revealed that EID‐1 specifically inhibited SF‐1, but not LRH‐1, ERRγ, or mCAR. Using yeast two hybrid and GST pull‐down assays, we determined that EID‐1 exhibited strong interaction with SF‐1. In addition, EID‐1 was determined to be colocalized with SF‐1 in mammalian living cells. EID‐1 was found to interact specifically with the AF‐2 domain of SF‐1, and competed with SRC‐1 to inhibit the transactivation of SF‐1. Physiologically, EID‐1 was expressed in the mouse testis, and EID‐1 expression in the testis was determined to decrease during the development of the mouse testis. The results of the present study suggest that EID‐1 can act as a repressor, regulating the function of SF‐1.