Cells navigate disordered networks through tension-guided pathways

Cells migrating through the extracellular matrix (ECM) generate contractile forces that mechanically signal their neighbors, guiding collective motion and enabling processes such as tissue morphogenesis, wound healing, and cancer invasion. Using a minimal computational model of motile contractile dipoles embedded in a disordered biopolymer network, we show how cell–ECM interactions drive the emergence of force chains, stress-bearing filament pathways that guide migration. Bulk stress rises rapidly and then evolves slowly due to rare tension-driven cell rearrangements, a process we quantify with a topological similarity index (TSI). We find that network connectivity and cell density jointly regulate stress, pore size, and the timescale of cells' topological position evolution, with higher connectivity or density suppressing migration by keeping cells in high-tension regions. Contractility inhibition and recovery simulations reveal that cells reoccupy pre-existing tension pathways determined by the ECM topology. To connect with experiments, we introduce an image similarity index (ISI), which quantifies the persistence of high-tension filament patterns in contracted networks. Together, our results highlight the dominant role of network disorder in governing the emergence of cells' spatial organization and provide a framework to directly compare computational models and experiments in mechanically and actively heterogeneous environments.