Cell movement relies on periodic edge protrusion, adhesion, and recovery. But whether these are regulated by biochemical or biomechanical processes has been an unsolved mystery.
Researchers from Columbia University, Université Bordeaux 2 and other research institutions found that myosin II pulled the lamellipodial actin network to bend in the back direction, retract the edges, and form new adhesion sites. The lamellipodial actin network is then separated from the edge and concentrated around myosin. When lamellipodial actin regenerates from the front end, the protrusion recovers and expands to the back end, reaching the newly assembled myosin and starting the next round of movement.
Evanescence and electron microscopy experiments show that when the adhesion is insufficient, upward bending will form a striated edge (ruffle). Related fluorescence and electron microscopy experiments show that the new lamellipodial will form a sticky, detachable actin layer on the lamellum. Therefore, periodic actin polymerization establishes a mechanical connection, and lamellipodium connects the myosin motor to the start of the support site, suggesting that the main function of the driving force is regulated by a biomechanical process.
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