The PI3K pathway balances self-renewal and differentiation of nephron progenitor cells through beta-catenin signalling.

Nils Lindstrom, Neil Carragher, Peter Hohenstein

Research output: Contribution to journalArticlepeer-review

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 β-catenin pathway. Therefore, the combined output of PI3K and other pathways fine-tunes the balance between self-renewal and differentiation in nephron progenitors.
Original languageEnglish
Pages (from-to)551-560
Number of pages10
JournalStem Cell Reports
Volume4
Issue number4
Early online date5 Mar 2015
DOIs
Publication statusPublished - 14 Apr 2015

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