Abstract
Studies in adrenocortical cells have implicated the orphan nuclear receptor SF-1 in the gene regulation of the steroid hydroxylases. We used targeted disruption of the Ftz-F1 gene, which encodes SF-1, to examine its role in intact mice. Despite normal survival in utero, all Ftz-F1 null animals died by postnatal day 8; these animals lacked adrenal glands and gonads and were severely deficient in corticosterone, supporting adrenocortical insufficiency as the probable cause of death. Male and female Ftz-F1 null mice had female internal genitalia, despite complete gonadal agenesis. These studies establish that the Ftz-F1 gene is essential for sexual differentiation and formation of the primary steroidogenic tissues.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adrenal Glands / embryology*
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Adrenocorticotropic Hormone / blood
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Animals
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Animals, Newborn
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Apoptosis
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Base Sequence
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Cell Movement
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Cloning, Molecular
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Corticosterone / blood
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / physiology
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Fallopian Tubes / embryology
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Female
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Fushi Tarazu Transcription Factors
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Germ Cells / cytology
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Gonads / embryology*
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Homeodomain Proteins
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Male
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Mice
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Mice, Knockout / genetics
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Molecular Sequence Data
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Receptors, Cytoplasmic and Nuclear / genetics*
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Receptors, Cytoplasmic and Nuclear / physiology
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Sex Differentiation / genetics*
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Steroidogenic Factor 1
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Transcription Factors / genetics*
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Transcription Factors / physiology
Substances
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DNA-Binding Proteins
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Fushi Tarazu Transcription Factors
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Homeodomain Proteins
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Receptors, Cytoplasmic and Nuclear
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Steroidogenic Factor 1
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Transcription Factors
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Adrenocorticotropic Hormone
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Corticosterone