Abstract
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 b-catenin pathway. Therefore, the combined output of PI3K and other pathways fine-tunes the balance between self-renewal and differentiation in nephron progenitors.
Original language | English (US) |
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Pages (from-to) | 551-560 |
Number of pages | 10 |
Journal | Stem cell reports |
Volume | 4 |
Issue number | 4 |
DOIs | |
State | Published - 2015 |
ASJC Scopus subject areas
- Biochemistry
- Genetics
- Developmental Biology
- Cell Biology