Ephrin B1 maintains apical adhesion of neural progenitors.

Fiche publication


Date publication

mai 2013

Journal

Development (Cambridge, England)

Auteurs

Membres identifiés du Cancéropôle Est :
Dr VITALE Nicolas, Dr TOTH Petra


Tous les auteurs :
Arvanitis DN, Béhar A, Tryoen-Tóth P, Bush JO, Jungas T, Vitale N, Davy A

Résumé

Apical neural progenitors are polarized cells for which the apical membrane is the site of cell-cell and cell-extracellular matrix adhesion events that are essential for maintaining the integrity of the developing neuroepithelium. Apical adhesion is important for several aspects of the nervous system development, including morphogenesis and neurogenesis, yet the mechanisms underlying its regulation remain poorly understood. Here, we show that ephrin B1, a cell surface protein that engages in cell signaling upon binding cognate Eph receptors, controls normal morphogenesis of the developing cortex. Efnb1-deficient embryos exhibit morphological alterations of the neuroepithelium that correlate with neural tube closure defects. Using loss-of-function experiments by ex vivo electroporation, we demonstrate that ephrin B1 is required in apical progenitors (APs) to maintain their apical adhesion. Mechanistically, we show that ephrin B1 controls cell-ECM adhesion by promoting apical localization of integrin β1 and we identify ADP-ribosylation factor 6 (Arf6) as an important effector of ephrin B1 reverse signaling in apical adhesion of APs. Our results provide evidence for an important role for ephrin B1 in maintaining the structural integrity of the developing cortex and highlight the importance of tightly controlling apical cell-ECM adhesion for neuroepithelial development.

Mots clés

ADP-Ribosylation Factors, metabolism, Animals, Body Patterning, Brain, embryology, Cell Adhesion, Cell Communication, Cell Membrane, metabolism, Cells, Cultured, Electroporation, Ephrin-B1, metabolism, Female, Male, Mice, Mice, Transgenic, Neural Tube, embryology, Neurons, cytology, Stem Cells, cytology, Time Factors

Référence

Development. 2013 May;140(10):2082-92