Hirata Hiroaki, Gupta Mukund, Vedula Sri Ram Krishna, Lim Chwee Teck, Ladoux Benoit, Sokabe Masahiro
Mechanobiology Institute, National University of Singapore, Singapore, Singapore.
Mechanobiology Institute, National University of Singapore, Singapore, Singapore Department of Biomedical Engineering, National University of Singapore, Singapore, Singapore Department of Mechanical Engineering, National University of Singapore, Singapore, Singapore.
EMBO Rep. 2015 Feb;16(2):250-7. doi: 10.15252/embr.201439140. Epub 2014 Dec 30.
Tensile forces generated by stress fibers drive signal transduction events at focal adhesions. Here, we report that stress fibers per se act as a platform for tension-induced activation of biochemical signals. The MAP kinase, ERK is activated on stress fibers in a myosin II-dependent manner. In myosin II-inhibited cells, uniaxial stretching of cell adhesion substrates restores ERK activation on stress fibers. By quantifying myosin II- or mechanical stretch-mediated tensile forces in individual stress fibers, we show that ERK activation on stress fibers correlates positively with tensile forces acting on the fibers, indicating stress fibers as a tension sensor in ERK activation. Myosin II-dependent ERK activation is also observed on actomyosin bundles connecting E-cadherin clusters, thus suggesting that actomyosin bundles, in general, work as a platform for tension-dependent ERK activation.
应力纤维产生的拉力驱动着黏着斑处的信号转导事件。在此，我们报告应力纤维本身作为一个平台，用于张力诱导的生化信号激活。丝裂原活化蛋白激酶ERK在应力纤维上以肌球蛋白II依赖的方式被激活。在肌球蛋白II受抑制的细胞中，细胞黏附底物的单轴拉伸可恢复应力纤维上的ERK激活。通过量化单个应力纤维中肌球蛋白II或机械拉伸介导的拉力，我们表明应力纤维上的ERK激活与作用于纤维的拉力呈正相关，这表明应力纤维是ERK激活中的张力传感器。在连接E-钙黏蛋白簇的肌动球蛋白束上也观察到了肌球蛋白II依赖的ERK激活，因此表明一般来说，肌动球蛋白束作为张力依赖的ERK激活的平台。
