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

Author:

Benham-Pyle Blair W.1,Pruitt Beth L.234,Nelson W. James145

Affiliation:

1. Program in Cancer Biology, Stanford University, Stanford, CA 94305, USA.

2. Stanford Cardiovascular Institute, Stanford University, Stanford, CA 94305, USA.

3. Department of Mechanical Engineering, Stanford University, Stanford, CA 94305, USA.

4. Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.

5. Department of Biology, Stanford University, Stanford, CA 94305, USA.

Abstract

Stretching cell sheets promotes proliferation Mechanical strain regulates the development, organization, and function of multicellular tissues. But how? Cadherins mechanically couple neighboring epithelial cells through extracellular interactions and sequester the transcription factors β-catenin and Yap1. To find out more, Benham-Pyle et al. stretched epithelial cell sheets. This mechanical strain induced rapid cell cycle reentry, DNA synthesis by sequential nuclear accumulation, and transcriptional activation of Yap1 and β-catenin. Thus, cell-cell junctions are mechanically responsive structural scaffolds providing signaling centers that coordinate transcriptional responses to externally applied force. Science , this issue p. 1024

Funder

NSF

NIH

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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