Endocrine Abstracts

The orphan nuclear receptor steroidogenic factor 1 (SF-1) initially was
isolated as a key regulator of the cytochrome P450 steroid hydroxylases.
Knockout mice lacking steroidogenic factor 1 (SF-1) have a complex
endocrine phenotype that encompasses adrenal and gonadal agenesis,
impaired expression of gonadotropins by pituitary gonadotropes, and
structural abnormalities of the ventromedial hypothalamic nucleus (VMH).
These multiple defects complicate efforts to define primary versus
secondary effects of SF-1 deficiency in different tissues. To generate
tissue-specific knockouts of SF-1, we expressed Cre recombinase driven
by several different promoters, thereby specifically inactivating a
modified SF-1 allele in the pituitary, ventromedial hypothalamic
nucleus, or the gonads. These tissue-specific SF-1 knockout mice provide
novel genetic models to explore the roles of SF-1 in specific cell
types. We also have used a 50 kb fragment from a SF-1 bacterial
artificial chromosome (BAC) that includes the 5'-flanking region, 1st
exon, first intron, and 32 nucleotides of the second exon to target
transgenic expression of enhanced green fluorescent protein (eGFP).
This SF-1/GFP transgene is expressed in the gonads, adrenal cortex, and
VMH, providing a novel tool to follow the development of SF-1 expressing
cells in multiple tissues.