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      WT-1 is required for early kidney development

      , , , , , ,

      Cell

      Elsevier BV

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          Abstract

          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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          Most cited references 31

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          Targeted mutation of the DNA methyltransferase gene results in embryonic lethality

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            Simplified mammalian DNA isolation procedure.

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              Effects of an Rb mutation in the mouse.

              The retinoblastoma gene is mutated in several types of human cancer and is the best characterized of the tumour-suppressor genes. A mouse strain has been constructed in which one allele of Rb is disrupted. These heterozygous animals are not predisposed to retinoblastoma, but some display pituitary tumours arising from cells in which the wild-type Rb allele is absent. Embryos homozygous for the mutation die between days 14 and 15 of gestation, exhibiting neuronal cell death and defective erythropoiesis.
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                Author and article information

                Journal
                Cell
                Cell
                Elsevier BV
                00928674
                August 1993
                August 1993
                : 74
                : 4
                : 679-691
                Article
                10.1016/0092-8674(93)90515-R
                8395349
                © 1993

                https://www.elsevier.com/tdm/userlicense/1.0/

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