FOCAL POINT  James Bear (left), Elizabeth Haynes (right), and colleagues reveal that a protein called GMFβ helps disassemble the branched actin networks generated by the Arp2/3 complex at the leading edge of migrating fibroblasts, promoting lamellipodial retraction and the cells’ ability to navigate towards adhesive directional cues. Compared with a control fibroblast (center), a cell lacking GMFβ (left) forms large lamellipodia that rarely retract. In contrast, a fibroblast overexpressing GMFβ (right) forms small, highly dynamic lamellipodia. In either case, the cells’ ability to follow a gradient of the extracellular matrix protein fibronectin is perturbed. / PHOTO COURTESY OF SREEJA ASOKAN

FOCAL POINT  James Bear (left), Elizabeth Haynes (right), and colleagues reveal that a protein called GMFβ helps disassemble the branched actin networks generated by the Arp2/3 complex at the leading edge of migrating fibroblasts, promoting lamellipodial retraction and the cells’ ability to navigate towards adhesive directional cues. Compared with a control fibroblast (center), a cell lacking GMFβ (left) forms large lamellipodia that rarely retract. In contrast, a fibroblast overexpressing GMFβ (right) forms small, highly dynamic lamellipodia. In either case, the cells’ ability to follow a gradient of the extracellular matrix protein fibronectin is perturbed.

PHOTO COURTESY OF SREEJA ASOKAN

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