Transitions from quiescence to collective migration in epithelia underlie wound healing and cancer invasion, yet their physical origin remains poorly understood. Here we show that quiescent epithelial monolayers store spatially contractile stresses that function as a form of mechanical memory. Upon serum-induced reactivation, these pre-stressed regions nucleate extensile asters that emit propagating polarity domain walls. Along these interfaces, topological defects are created, advected and annihilated, leading to defect coarsening with faster kinetics than by elastic interactions. An active elastic model quantitatively reproduces the observed dynamics and identifies stored stress as the origin of rapid topological reorganization. Our results establish a mechanism in which mechanical memory in quiescent epithelia triggers active stress release, driving collective migration via rapid topological ordering, distinct from conventional unjamming and flocking transitions.

生成讲解博客的中文版本

生成AI智能校验的中文版本