MAPK/ERK通路
肌球蛋白
应力纤维
张力(地质)
生物物理学
压力(语言学)
细胞生物学
材料科学
极限抗拉强度
焦点粘着
肌球蛋白轻链激酶
粘附
化学
作者
Hiroaki Hirata,Mukund Gupta,Sri Ram Krishna Vedula,Chwee Teck Lim,Benoit Ladoux,Masahiro Sokabe
标识
DOI:10.15252/embr.201439140
摘要
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.
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