Figure 1.
Panel A: A diagram showing tissue under tension with tricellular junctions (TCJs) and bicellular junctions (BCJs) highlighted. Panel B: A series of diagrams illustrating the recruitment of the adhesion protein Canoe to TCJs in a force-dependent manner, contributing to adhesion strengthening. Panel C: Diagrams showing the role of Mbt/PAK in organizing Canoe into optimal-sized condensates for transport to TCJs, with conditions of hypo-condensation and hyper-condensation leading to inefficient transport. Panel D: Diagrams depicting the restoration of adhesion following cell division at the Drosophila ventral midline, with hyper-condensation of Canoe resulting in epithelial gaps due to defective adhesion reinforcement.
Canoe/Afadin is delivered via edge-vertex flow to epithelial cell–cell junctions under stress. (A) Epithelial cells under tension exhibit reinforced adhesion at TCJs, relative to BCJs. (B) The adhesion protein Canoe is recruited to TCJs in a force-dependent manner, contributing to adhesion strengthening. (C) Mbt/PAK helps organize Canoe into optimal-sized condensates that are transported to TCJs. Hypo-condensation or hyper-condensation of Canoe results in inefficient transport and lack of adhesion reinforcement. (D) Following cell division at the Drosophila ventral midline, Mbt/PAK and Canoe restore adhesion. When Canoe is hyper-condensed due to loss of Mbt/PAK, epithelial gaps emerge due to defective adhesion reinforcement.