FOCAL POINT  Andrea McClatchey (left), Christine Chiasson-MacKenzie (right), and colleagues describe a novel mechanism by which the tumor suppressor Merlin/NF2 mediates contact-dependent inhibition of proliferation. By limiting the recruitment of the actin-binding protein Ezrin to the apical cell cortex, Merlin regulates the mechanical forces transduced between cell–cell contacts and the cortical cytoskeleton, allowing the EGFR to be immobilized and inhibited when epithelial cells reach confluency. In wild-type cells (center), myosin IIA (green) is uniformly distributed across the apical cortex, but in the absence of Merlin (right), it coalesces into puncta, an indicator of increased contractility and excess tension on cell–cell junctions (red). / PHOTO COURTESY OF BRIAN BRANNIGAN

FOCAL POINT  Andrea McClatchey (left), Christine Chiasson-MacKenzie (right), and colleagues describe a novel mechanism by which the tumor suppressor Merlin/NF2 mediates contact-dependent inhibition of proliferation. By limiting the recruitment of the actin-binding protein Ezrin to the apical cell cortex, Merlin regulates the mechanical forces transduced between cell–cell contacts and the cortical cytoskeleton, allowing the EGFR to be immobilized and inhibited when epithelial cells reach confluency. In wild-type cells (center), myosin IIA (green) is uniformly distributed across the apical cortex, but in the absence of Merlin (right), it coalesces into puncta, an indicator of increased contractility and excess tension on cell–cell junctions (red).

PHOTO COURTESY OF BRIAN BRANNIGAN

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