title: Actomyosin bundles serve as a tension sensor and a platform for ERK activation.
abstract: 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.
authors.affiliation: Mechanobiology Institute, National University of Singapore, Singapore, Singapore.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Hirata
authors.affiliation: Mechanobiology Institute, National University of Singapore, Singapore, Singapore.
authors.forename: Mukund
authors.initials: M
authors.lastname: Gupta
authors.affiliation: Mechanobiology Institute, National University of Singapore, Singapore, Singapore.
authors.forename: Sri Ram Krishna
authors.initials: SR
authors.lastname: Vedula
authors.affiliation: 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.
authors.forename: Chwee Teck
authors.initials: CT
authors.lastname: Lim
authors.affiliation: Mechanobiology Institute, National University of Singapore, Singapore, Singapore Institut Jacques Monod (IJM), CNRS UMR 7592 Université Paris Diderot, Paris, France.
authors.forename: Benoit
authors.initials: B
authors.lastname: Ladoux
authors.affiliation: Mechanobiology Institute, National University of Singapore, Singapore, Singapore Mechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya, Japan msokabe@med.nagoya-u.ac.jp.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Sokabe
mesh_terms: D000205:Actomyosin / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D022001:Focal Adhesions / Q000378:metabolism; D006801:Humans; D040542:Mechanotransduction, Cellular / Q000502:physiology; D051379:Mice; D024462:Myosin Type II / Q000378:metabolism; D041681:NIH 3T3 Cells; D022502:Stress Fibers / Q000378:metabolism*; D013718:Tensile Strength / Q000502:physiology
chemical_list: D000205:Actomyosin; D048049:Extracellular Signal-Regulated MAP Kinases; D024462:Myosin Type II
keywords: contractility; mechanotransduction; stress fiber; tensile force