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      Sox9 expression during gonadal development implies a conserved role for the gene in testis differentiation in mammals and birds.

      Nature genetics

      Amino Acid Sequence, Animals, Base Sequence, Cell Nucleus, metabolism, Chickens, DNA Primers, DNA-Binding Proteins, genetics, Female, Gene Expression, High Mobility Group Proteins, physiology, Male, Mammals, Mice, Molecular Sequence Data, Nuclear Proteins, SOX9 Transcription Factor, Sertoli Cells, Sex Differentiation, Sex-Determining Region Y Protein, Testis, growth & development, Transcription Factors, X Chromosome

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          Abstract

          Heterozygous mutations in SOX9 lead to a human dwarfism syndrome, Campomelic dysplasia. Consistent with a role in sex determination, we find that Sox9 expression closely follows differentiation of Sertoli cells in the mouse testis, in experimental sex reversal when fetal ovaries are grafted to adult kidneys and in the chick where there is no evidence for a Sry gene. Our results imply that Sox9 plays an essential role in sex determination, possibly immediately downstream of Sry in mammals, and that it functions as a critical Sertoli cell differentiation factor, perhaps in all vertebrates.

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          Most cited references41

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          Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.

          A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described. The method provides a pure preparation of undegraded RNA in high yield and can be completed within 4 h. It is particularly useful for processing large numbers of samples and for isolation of RNA from minute quantities of cells or tissue samples.
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            A series of normal stages in the development of the chick embryo

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              WT-1 is required for early kidney development.

              In humans, germline mutations of the WT-1 tumor suppressor gene are associated with both Wilms' tumors and urogenital malformations. To develop a model system for the molecular analysis of urogenital development, we introduced a mutation into the murine WT-1 tumor suppressor gene by gene targeting in embryonic stem cells. The mutation resulted in embryonic lethality in homozygotes, and examination of mutant embryos revealed a failure of kidney and gonad development. Specifically, at day 11 of gestation, the cells of the metanephric blastema underwent apoptosis, the ureteric bud failed to grow out from the Wolffian duct, and the inductive events that lead to formation of the metanephric kidney did not occur. In addition, the mutation caused abnormal development of the mesothelium, heart, and lungs. Our results establish a crucial role for WT-1 in early urogenital development.
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                Author and article information

                Journal
                8782821
                10.1038/ng0996-62

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