麻豆AV

Cells are truly the ultimate 鈥渟mart-material鈥� fine-tuning their mechanical properties to match the mechanical demands of their environments. Such plasticity of cell mechanics relies heavily on the spatiotemporal regulation of the actomyosin cytoskeleton, and plays a protective role safeguarding cells against mechanical damage. Yet, mechanisms of the adaptive changes in cell mechanics remain elusive. In this presentation, I will report a new mechanism whereby mechanically activated actin elongation factor mDia1 controls the dynamics of actin polymerization at focal adhesions, force bearing linkages between the actin cytoskeleton and extracellular matrix. By combining live-cell imaging with mathematical modelling, we show that actin polymerization at focal adhesions exhibits pulsatile dynamics where the spikes of mDia1 activity are triggered by cell-generated contractile forces. We show that suppression of mDia1-mediated actin polymerization at focal adhesions results in two-fold increase in mechanical tension on the stress fibers. This elevated tension leads to an increased frequency of spontaneous stress fiber damage and decreased efficiency of zyxin-mediated stress fiber repair. We conclude that tension-controlled actin polymerization at focal adhesions acts as a safety valve dampening excessive mechanical tension on the actin cytoskeleton and safeguarding stress fibers against mechanical damage.

This seminar will be given online via Zoom. Details in attached poster.