
SUMMARYThe fluid-mosaic model posits a liquid-like plasma membrane, which can flow in response to tension gradients. It is widely assumed that membrane flow transmits local changes in membrane tension across the cell in milliseconds. This conjectured signaling mechanism has been invoked to explain how cells coordinate changes in shape, motility, and vesicle fusion, but the underlying propagation has never been observed. Here we show that propagation of membrane tension occurs quickly in cell-attached blebs, but is largely suppressed in intact cells. The failure of tension to propagate in cells is explained by a fluid dynamical model that incorporates the flow resistance from cytoskeleton-bound transmembrane proteins. In primary endothelial cells, local increases in membrane tension lead only to local activation of mechanosensitive ion channels and to local vesicle fusion. Thus membrane tension is not a mediator of long-range intra-cellular signaling, but local variations in tension mediate distinct processes in sub-cellular domains.
Cell Membrane, Models, Biological, Ion Channels, Madin Darby Canine Kidney Cells, Rats, Mice, Dogs, NIH 3T3 Cells, Animals, Humans, Cytoskeleton, HeLa Cells, Signal Transduction
Cell Membrane, Models, Biological, Ion Channels, Madin Darby Canine Kidney Cells, Rats, Mice, Dogs, NIH 3T3 Cells, Animals, Humans, Cytoskeleton, HeLa Cells, Signal Transduction
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