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Steroidogenic Factor 1: A Key Determinant of Endocrine Development and Function

Departments of Medicine and Pharmacology and the Howard Hughes Medical Institute (K.L.P.), Duke University Medical Center, Durham, North Carolina 27710; and the Banting and Best Department of Medical Research (B.P.S.), University of Toronto, Toronto, Canada M5G 1L6

I. Introduction

II. The Initial Identification of SF-1 as a Key Determinant of Steroid Hormone Biosynthesis

A. Overview of steroidogenesis

B. SF-1 and the regulation of steroidogenesis

C. Cloning and structural characterization of SF-1

1. Structural features of SF-1

2. Multiple transcripts are encoded by the gene encoding SF-1

3. The gene encoding SF-1 is evolutionarily conserved in vertebrates and invertebrates

III. Characterization of Sites of SF-1 Expression and Identification of Its Target Genes

A. Profiles of SF-1 expression

1. Adult steroidogenic tissues

2. Embryonic steroidogenic tissues

3. Other sites of SF-1 expression

B. Target genes regulated by SF-1

1. Steroidogenic cells

2. Sertoli cells

3. Gonadotropes

4. VMH

IV. The Roles Of SF-1 in Vivo: Targeted Gene Disruption to Create SF-1 Knockout Mice

A. General features of the SF-1 knockout mice

B. Primary steroidogenic tissues in SF-1 knockout mice

C. Pituitary and hypothalamic defects in SF-1 knockout mice

V. Perspectives and Future Directions

A. What are the roles of the various transcripts encoded by the Ftz-F1 gene?

B. Does a ligand mediate SF-1 transcriptional activation?

C. Where does SF-1 fit within hierarchical cascades of endocrine development?

1. Which other genes also contribute to tissue-selective expression of SF-1 target genes?

2. Which target genes of SF-1 mediate its key roles in maintaining the adrenal glands, gonads, and VMH?

3. What mechanisms regulate the expression of SF-1?

4. How is SF-1 related to other genes whose disruptions lead to phenotypes that resemble the SF-1 knockout mice?

D. Do other transcription factors/nuclear receptors serve dual roles in development and maintenance of the differentiated phenotype?

VI. Conclusion