Journal
STEM CELL REPORTS
Volume 4, Issue 4, Pages 551-560Publisher
CELL PRESS
DOI: 10.1016/j.stemcr.2015.01.021
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Funding
- National Centre for Replacement, Refinement and Reduction of Animals in Research [94808]
- Biotechnology and Biological Sciences Research Council [BB/J004316/1]
- BBSRC [BBS/E/D/20221657] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/D/20221657] Funding Source: researchfish
- National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC3Rs) [NC/K500549/1] Funding Source: researchfish
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Nephron progenitor cells differentiate to form nephrons during embryonic kidney development. In contrast, self-renewal maintains progenitor numbers and premature depletion leads to impaired kidney function. Here we analyze the PI3K pathway as a point of convergence for the multiple pathways that are known to control self-renewal in the kidney. We demonstrate that a reduction in PI3K signaling triggers premature differentiation of the progenitors and activates a differentiation program that precedes the mesenchymal-to-epithelial transition through ectopic activation of the beta-catenin pathway. Therefore, the combined output of PI3K and other pathways fine-tunes the balance between self-renewal and differentiation in nephron progenitors.
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