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      Cell adhesion. Mechanical strain induces E-cadherin-dependent Yap1 and β-catenin activation to drive cell cycle entry.

      1 , 2 , 3

      Science (New York, N.Y.)

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          Abstract

          Mechanical strain regulates the development, organization, and function of multicellular tissues, but mechanisms linking mechanical strain and cell-cell junction proteins to cellular responses are poorly understood. Here, we showed that mechanical strain applied to quiescent epithelial cells induced rapid cell cycle reentry, mediated by independent nuclear accumulation and transcriptional activity of first Yap1 and then β-catenin. Inhibition of Yap1- and β-catenin-mediated transcription blocked cell cycle reentry and progression through G1 into S phase, respectively. Maintenance of quiescence, Yap1 nuclear exclusion, and β-catenin transcriptional responses to mechanical strain required E-cadherin extracellular engagement. Thus, activation of Yap1 and β-catenin may represent a master regulator of mechanical strain-induced cell proliferation, and cadherins provide signaling centers required for cellular responses to externally applied force.

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          Author and article information

          Journal
          Science
          Science (New York, N.Y.)
          1095-9203
          0036-8075
          May 29 2015
          : 348
          : 6238
          Affiliations
          [1 ] Program in Cancer Biology, Stanford University, Stanford, CA 94305, USA.
          [2 ] Stanford Cardiovascular Institute, Stanford University, Stanford, CA 94305, USA. Department of Mechanical Engineering, Stanford University, Stanford, CA 94305, USA. Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.
          [3 ] Program in Cancer Biology, Stanford University, Stanford, CA 94305, USA. Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA. Department of Biology, Stanford University, Stanford, CA 94305, USA. wjnelson@stanford.edu.
          Article
          348/6238/1024 NIHMS720077
          10.1126/science.aaa4559
          26023140
          Copyright © 2015, American Association for the Advancement of Science.

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