Edge-vertex flow enables rapid adhesion reinforcement under tension

A general mechanism to maintain epithelial integrity during tissue movements is to couple adhesion strength with mechanical force. Mechanosensitive proteins are recruited to cell-cell contacts to reinforce membrane-cortex linkage in response to elevated tension. However, how protein recruitment achieves necessary speed and precision to match the instant nature of force remains unknown. Here we identify a direct "edge-to-vertex" transport mechanism that couples the flow of the adhesion protein Canoe/Afadin to pulsatile actomyosin dynamics, ensuring that adhesion is reinforced precisely where and when force is applied. Genetically, this mechanosensitive transport is gated by kinase-independent activities of Mbt/PAK. In its absence, Canoe/Afadin forms aberrant elliptical condensates at cell edges, becoming unresponsive to mechanical cues. Remarkably, these condensates are dissolved by a simple, physiological increase in temperature, which restores directional protein flow and rescues adhesion-bypassing the genetic requirement of Mbt/PAK. Lastly, we demonstrate that transport efficiency is governed by cortical mobility threshold, fine-tuned through Canoe/Afadin condensation. These results identify a force-coupled transport strategy to ensure adhesion-tension coupling with spatial and temporal precision in living tissues.