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- W2796005914 abstract "Adherent cells actively sense the mechanical stiffness of their extracellular matrix (ECM) by exerting traction force through focal adhesions (FAs), which are integrin-based protein assemblies. Also, FAs control cell spreading, proliferation, survival, differentiation, and migration. FA-mediated mechanosensation underlies cell durotaxis - the tendency of most cell types to migrate toward stiffer microenvironment. Strikingly, FA-mediated traction forces oscillate in time and space, and this oscillation governs durotaxis. The interactions underlying this intriguing spatio-temporal pattern of FA traction force are unknown, as are the contributions of these interactions to this mechanosensation. To address these questions, we established the first coherent, experimentally validated model of FA formation. The model integrated the spatiotemporal coordination between a branched actin network and stress fibers during FA growth. Our model predicted that retrograde flux of branched actin network contributed to a traction peak near the FA distal tip and that stress fiber-mediated actomyosin contractility generated a second traction peak near the FA center. Furthermore, a negative feedback loop involving formin-mediated stress fiber elongation and actomyosin contractility developed and resulted in oscillation of the center traction peak. This oscillation competed with the distal traction peak, and the competition underpinned oscillation of the FA traction maximum in time and space. More importantly, this negative feedback loop broadened the substrate stiffness range, over which the FAs could accurately adapt with traction force generation. Our findings shed light on the fundamental mechanism of FA mechanosensation and durotaxis." @default.
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- W2796005914 date "2016-03-15" @default.
- W2796005914 modified "2023-09-27" @default.
- W2796005914 title "Two distinct actin networks mediate traction oscillations to confer mechanosensitivity of focal adhesions" @default.
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