| Cerebral cortical precursors reside in a neuroepithelial cell layer that regulates their proliferation and differentiation. We initially demonstrate that alphaE-catenin is preferentially expressed within these neural precursors, while alphaN-catenin is predominantly expressed in differentiated neurons. Genetic deletion of alphaE-catenin within neural precursors causes global disruptions in epithelial architecture, loss of lamination, and hyperproliferation. However cell autonomous reduction of alphaE-catenin in the background of normal precursors in vivo causes cells to prematurely exit the cell cycle, differentiate into neurons, and migrate to the cortical plate, while normal neighboring precursors are unaffected. Mechanistically, alphaE-catenin likely regulates cortical precursor differentiation by maintaining beta-catenin signaling, as reduction of alphaE-catenin leads to reduction of beta-catenin signaling in vivo. These results demonstrate that, at the cellular level, alphaE-catenin serves to maintain precursors in the proliferative ventricular zone, and suggest an unexpected function for alphaE-catenin in preserving beta-catenin signaling during cortical development. |
