Filament mechanics and turnover organize dynamic load bearing structures in a cellular-scale model of the actomyosin cortex

The actomyosin cortex controls cell shape and movement by generating and transmitting contractile forces. Its actin filament (AF) network adopts diverse spatial organizations, while spatially biased contractility drives cortical flow that transports components and reorganizes the network. However, how turnover and spatial redistribution organize and maintain tension-bearing structures in a dynamic steady state, and how localized contractility reorganizes them through flow, remain unclear. We developed a cellular-scale discrete model of the actomyosin cortex representing AFs, cross-linkers, and myosin minifilaments. Local surface stress was reconstructed from discrete-element internal forces based on continuum mechanics. We related cortical tension to component abundance, tensile deformation, AF orientation, turnover, and network connectivity, and compared different AF disassembly, relocation, and myosin-localization mechanisms. Simulations produced a heterogeneous, network-like distribution of local cortical tension. Tensile energy per element correlated more strongly with local tension than component abundance, with the strongest correlation for AFs. Highly stretched AFs preferentially occurred in high-tension regions and aligned with the first-principal-tension orientation, indicating anisotropic load-bearing pathways. Despite continuous component replacement and reorganization of local tension patterns, global AF-network connectivity and cell-scale cortical tension were maintained. The characteristic time of tension-pattern reorganization was closest to the persistence time of myosin, suggesting an association between myosin dynamics and rapid force redistribution. AF relocation to low-density regions replenished spatial gaps, whereas bending-dependent disassembly limited the accumulation of strongly deformed AFs. Direct myosin localization and AF accumulation produced comparable equatorward cortical flows but differed in the spatial organization of the tension-bearing network. Collectively, these results demonstrate that cellular-scale cortical tension is organized not only by component abundance but also by filament-scale mechanical loading, AF orientation, and network connectivity.