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Department of Reproductive Medicine (A.N.H., P.L.M.) Department of Neuroscience and the Center for Molecular Genetics (P.L.M.) University of California, San Diego La Jolla, California 92093-0674
Tissue-specific expression of the mammalian FTZ-F1
gene is essential for adrenal and gonadal development and sexual
differentiation. The FTZ-F1 gene encodes an orphan nuclear receptor,
termed SF-1 (steroidogenic factor-1) or Ad4BP, which is a primary
transcriptional regulator of several hormone and steroidogenic enzyme
genes that are critical for normal physiological function of the
hypothalamic-pituitary-gonadal axis in reproduction. The objective of
the current study is to understand the molecular mechanisms underlying
transcriptional regulation of SF-1 gene expression in the pituitary. We
have studied a series of deletion and point mutations in the SF-1
promoter region for transcriptional activity in 
T3–1 and LßT2
(pituitary gonadotrope), CV-1, JEG-3, and Y1 (adrenocortical) cell
lines. Our results indicate that maximal expression of the SF-1
promoter in all cell types requires an E box element at -82/-77. This
E box sequence (CACGTG) is identical to the binding element for USF
(upstream stimulatory factor), a member of the helix-loop-helix family
of transcription factors. Studies of the SF-1 gene E box element using
gel mobility shift and antibody supershift assays indicate that USF may
be a key transcriptional regulator of SF-1 gene expression.
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