Abstract

Neutrophils leverage feedback between mechanical forces and biochemical signaling to guide their polarity and motility during immune surveillance. These cells move by establishing a single leading front which protrudes and a back that contracts and follows the front. We recently found that cell surface tension-based communication between actin protrusions (relayed by the PLD2/mTORC2 pathway) is responsible for long-range competition between protrusions for proper control of polarity and movement.

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