LAUSR

Arp2/3 complex is thought to be the primary protrusive force generator in cell migration by controlling the assembly and turnover of the branched filament network that pushes the leading edge of moving cells forward. However, mouse fibroblasts without functional Arp2/3 complex migrate at rates similar to wild-type cells. Correlative fluorescence and large-scale cellular cryo-tomography studies combined with automated actin-network analysis allow examining the effect of the absence of functional Arp2/3 complex on the architecture of actin networks in fibroblast cells at the single-filament scale. Because Arp2/3 complex can only fulfill its function in the cell when all seven subunits are assembled, genetic elimination of the ARPC3 subunit ensures that functional Arp2/3 complex is absent in the ARPC3-/- cells versus the wild type. Quantitative analysis at the single filament scale of these isogenic cell lines suggests that the role of Arp2/3 complex in cell motility contains, in addition to generating dendritic actin networks at the leading edge and filopodia regulation, an element that is responsible for the fine-tuning of actin-bundle morphology at the cell periphery as well as in protrusions.