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      Wilms' tumor 1 and Dax-1 modulate the orphan nuclear receptor SF-1 in sex-specific gene expression.

      Cell

      Animals, Anti-Mullerian Hormone, Cell Line, DAX-1 Orphan Nuclear Receptor, DNA, metabolism, DNA-Binding Proteins, analysis, genetics, physiology, Disorders of Sex Development, Female, Fushi Tarazu Transcription Factors, Gene Expression Regulation, Developmental, Genes, Wilms Tumor, Glycoproteins, Growth Inhibitors, Homeodomain Proteins, Humans, Male, Models, Genetic, Mutation, Organ Specificity, Ovary, chemistry, embryology, Placenta, cytology, RNA, Messenger, Rats, Receptors, Cytoplasmic and Nuclear, Receptors, Retinoic Acid, Repressor Proteins, Sex Determination Processes, Steroidogenic Factor 1, Testicular Hormones, Testis, Transcription Factors, Transcriptional Activation, WT1 Proteins

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          Abstract

          Products of steroidogenic factor 1 (SF-1) and Wilms' tumor 1 (WT1) genes are essential for mammalian gonadogenesis prior to sexual differentiation. In males, SF-1 participates in sexual development by regulating expression of the polypeptide hormone Müllerian inhibiting substance (MIS). Here, we show that WT1 -KTS isoforms associate and synergize with SF-1 to promote MIS expression. In contrast, WT1 missense mutations, associated with male pseudohermaphroditism in Denys-Drash syndrome, fail to synergize with SF-1. Additionally, the X-linked, candidate dosage-sensitive sex-reversal gene, Dax-1, antagonizes synergy between SF-1 and WT1, most likely through a direct interaction with SF-1. We propose that WT1 and Dax-1 functionally oppose each other in testis development by modulating SF-1-mediated transactivation.

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          Journal
          9590178
          10.1016/S0092-8674(00)81172-1

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