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Cell-extrinsic mechanical forces restore neutrophil polarization in the absence of branched actin assembly

For directed movement, cells must constrain protrusions to a limited region of their surface. Both the local positive and global negative feedback loops that generate polarity are thought to be regulated by actin polymerization. However, the types of actin networks contributing to feedback and the underlying mechanisms remain unclear. Here we show that branched actin networks assembled by Arp2/3 and WAVE complex are essential for proper neutrophil polarity and motility in unconfined environments. In contrast, confined cells use a distinct mode of leading-edge advance and polarization whose regulatory positive and negative feedback loops do not depend on branched actin networks. By applying physical perturbations to the plasma membrane, we find that the long-range inhibitor enabling front competition does not solely respond to changes in membrane tension. This work revises our understanding of the core neutrophil polarity network and indicates that cells have distinct molecular circuits for polarity that dominate in different environments.