| Cells must overcome resistance when moving through tissue during metastasis or wound healing. The forces they can withstand are determined by their force-velocity relation, which has been measured for keratocytes but remains unexplained. We present a mechanism explaining that relation and its changes upon application of drugs that hinder actin polymerization or actomyosin based contractility. Already small opposing forces slow down lamellipodium motion by three orders of magnitude due to the delicate force balance at its leading edge. Increasing external forces accelerates actin gel retrograde flow until it compensates for polymerization and cell motion stalls. Subsequently, the force-velocity relation spirals transiently around the stall force due to adaptation to the stalled state. It reflects the force sensitivity of the lamellipodium leading edge and retrograde flow. |
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