A mechanosensitive RhoA pathway that protects epithelia against acute tensile stress
Date
2018
Authors
Acharya, B.R.
Nestor Bergmann, A.
Liang, X.
Gupta, S.
Duszyc, K.
Gauquelin, E.
Gomez, G.A.
Budnar, S.
Marcq, P.
Jensen, O.E.
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Advisors
Journal Title
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Type:
Journal article
Citation
Developmental Cell, 2018; 47(4):439-452
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Abstract
Adherens junctions are tensile structures that couple epithelial cells together. Junctional tension can arise from cell-intrinsic application of contractility or from the cell-extrinsic forces of tissue movement. Here, we report a mechanosensitive signaling pathway that activates RhoA at adherens junctions to preserve epithelial integrity in response to acute tensile stress. We identify Myosin VI as the force sensor, whose association with E-cadherin is enhanced when junctional tension is increased by mechanical monolayer stress. Myosin VI promotes recruitment of the heterotrimeric G alpha 12 protein to E-cadherin, where it signals for p114 RhoGEF to activate RhoA. Despite its potential to stimulate junctional actomyosin and further increase contractility, tension-activated RhoA signaling is necessary to preserve epithelial integrity. This is explained by an increase in tensile strength, especially at the multicellular vertices of junctions, that is due to mDia1-mediated actin assembly.
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Link to a related website: http://www.cell.com/article/S1534580718307767/pdf, Open Access via Unpaywall
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Copyright 2018 Elsevier