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Membrane tension controls adhesion positioning at the leading edge of cells.

Bruno PontesPascale MonzoLaurent GoleAnabel-Lise Le RouxAnita Joanna KosmalskaZhi Yang TamWeiwei LuoSophie KanVirgile ViasnoffPere Roca-CusachsLisa Tucker-KelloggNils C Gauthier
Published in: The Journal of cell biology (2017)
Cell migration is dependent on adhesion dynamics and actin cytoskeleton remodeling at the leading edge. These events may be physically constrained by the plasma membrane. Here, we show that the mechanical signal produced by an increase in plasma membrane tension triggers the positioning of new rows of adhesions at the leading edge. During protrusion, as membrane tension increases, velocity slows, and the lamellipodium buckles upward in a myosin II-independent manner. The buckling occurs between the front of the lamellipodium, where nascent adhesions are positioned in rows, and the base of the lamellipodium, where a vinculin-dependent clutch couples actin to previously positioned adhesions. As membrane tension decreases, protrusion resumes and buckling disappears, until the next cycle. We propose that the mechanical signal of membrane tension exerts upstream control in mechanotransduction by periodically compressing and relaxing the lamellipodium, leading to the positioning of adhesions at the leading edge of cells.
Keyphrases
  • cell migration
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  • cell cycle arrest
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  • pi k akt
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