TY - JOUR T1 - Distinct Rap1 activity states control the extent of epithelial invagination via α-catenin. JF - Dev Cell Y1 - 2013 A1 - Wang, Yu-Chiun A1 - Khan, Zia A1 - Wieschaus, Eric F KW - Actins KW - alpha Catenin KW - Animals KW - Cell Adhesion KW - Cell Adhesion Molecules KW - Cell Membrane KW - Cell Shape KW - Drosophila KW - Drosophila Proteins KW - Embryo, Nonmammalian KW - Enzyme Activation KW - Epithelial Cells KW - Genes, Insect KW - Green Fluorescent Proteins KW - GTP Phosphohydrolases KW - GTPase-Activating Proteins KW - Intercellular Junctions KW - RNA Interference KW - Time factors KW - Time-Lapse Imaging AB -

Localized cell shape change initiates epithelial folding, while neighboring cell invagination determines the final depth of an epithelial fold. The mechanism that controls the extent of invagination remains unknown. During Drosophila gastrulation, a higher number of cells undergo invagination to form the deep posterior dorsal fold, whereas far fewer cells become incorporated into the initially very similar anterior dorsal fold. We find that a decrease in α-catenin activity causes the anterior fold to invaginate as extensively as the posterior fold. In contrast, constitutive activation of the small GTPase Rap1 restricts invagination of both dorsal folds in an α-catenin-dependent manner. Rap1 activity appears spatially modulated by Rapgap1, whose expression levels are high in the cells that flank the posterior fold but low in the anterior fold. We propose a model whereby distinct activity states of Rap1 modulate α-catenin-dependent coupling between junctions and actin to control the extent of epithelial invagination.

VL - 25 CP - 3 M3 - 10.1016/j.devcel.2013.04.002 ER -