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- W2001019904 abstract "The kidney develops through reciprocal interactions between two precursor tissues: the metanephric mesenchyme and the ureteric bud. We previously reported that the zinc finger protein Sall1 is essential for ureteric bud attraction toward the mesenchyme. We also demonstrated that multipotent nephron progenitors that form colonies upon Wnt4 stimulation, and which strongly express Sall1, exist in the metanephric mesenchyme; these cells can partially reconstitute a three-dimensional structure in an organ culture setting. Here we show that Kif-k, a kinesin family gene, is a downstream target of Sall1 and that disruption of this gene causes kidney agenesis because of impaired ureteric bud attraction. In the Kif-k-null metanephros, compact adhesion between mesenchymal cells adjacent to the ureteric buds and the polarized distribution of integrin α8 were impaired, resulting in failed maintenance of Gdnf, a critical ureteric bud attractant. Overexpression of Kif-k in vitro caused increased cell adhesion through interactions with non-muscle myosin. Thus Kif-k is essential for kidney development because it regulates the adhesion of mesenchymal cells in contact with ureteric buds. Upon induction by ureteric buds, successive activation of Wnt4 and Notch2 generates nephrons from the nephron progenitors in the metanephric mesenchyme. Mesenchymal-to-epithelial transition requires Wnt4, and normal development of the proximal nephron (epithelia of glomeruli and proximal tubules) requires Notch2. It is unknown, however, whether Notch2 dictates the fate of the proximal nephron directly. Thus, we generated a mutant strain of mice with activated Notch2 in Six2-containing nephron progenitor cells of the metanephric mesenchyme. Notch2 activation did not skew the cell fate toward the proximal nephron but resulted in severe kidney dysgenesis and depletion of Six2-positive progenitors. We observed ectopic expression of Wnt4 and premature tubule formation, similar to the phenotype of Six2-deficient mice. Taken together, these data suggest that a positive feedback loop exists between Notch2 and Wnt4, and that Notch2 stabilizes, rather than dictates, nephron fate by shutting down the maintenance of undifferentiated progenitor cells, thereby depleting this population." @default.
- W2001019904 created "2016-06-24" @default.
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- W2001019904 date "2010-11-01" @default.
- W2001019904 modified "2023-09-26" @default.
- W2001019904 title "O29. Nephron progenitors in the embryonic kidney" @default.
- W2001019904 doi "https://doi.org/10.1016/j.diff.2010.09.172" @default.
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