Hepatocyte growth factor acutely perturbs actin filament anchorage at the epithelial zonula adherens

Mangold, Sabine, Wu, Selwin K., Norwood, Suzanne J., Collins, Brett M., Hamilton, Nicholas A., Thorn, Peter and Yap, Alpha S. (2011) Hepatocyte growth factor acutely perturbs actin filament anchorage at the epithelial zonula adherens. Current Biology, 21 6: 503-507. doi:10.1016/j.cub.2011.02.018


Author Mangold, Sabine
Wu, Selwin K.
Norwood, Suzanne J.
Collins, Brett M.
Hamilton, Nicholas A.
Thorn, Peter
Yap, Alpha S.
Title Hepatocyte growth factor acutely perturbs actin filament anchorage at the epithelial zonula adherens
Journal name Current Biology   Check publisher's open access policy
ISSN 0960-9822
1879-0445
Publication date 2011-03-22
Sub-type Article (original research)
DOI 10.1016/j.cub.2011.02.018
Volume 21
Issue 6
Start page 503
End page 507
Total pages 5
Place of publication Cambridge, MA, United States
Publisher Cell Press
Collection year 2012
Language eng
Abstract Cadherin adhesion molecules function in close cooperation with the actin cytoskeleton. At the zonula adherens (ZA) of polarized epithelial cells, E-cadherin adhesion induces the cortical recruitment of many key cytoskeletal regulators, which act in a dynamic integrated system to regulate junctional integrity and cell-cell interactions [[1], [2] and [3]]. This capacity for the cytoskeleton to support the ZA carries the implication that regulators of the junctional cytoskeleton might also be targeted to perturb junctional integrity. In this report, we now provide evidence for this hypothesis. We show that hepatocyte growth factor (HGF), which is well-known to disrupt cell-cell interactions, acutely perturbs ZA integrity much more rapidly than generally appreciated. This is accompanied by significant loss of junctional F-actin, a process that reflects loss of filament anchorage at the junctions. We demonstrate that this involves uncoupling of the unconventional motor myosin VI from junctional E-cadherin, a novel effect of HGF that is mediated by intracellular calcium. We conclude that regulators of the junctional cytoskeleton are likely to be major targets for cadherin junctions to be acutely modulated in development and perturbed in disease.
Keyword Myosin-VI
Scatter factor
Adhesive contacts
Cell contact
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2012 Collection
School of Biomedical Sciences Publications
Institute for Molecular Bioscience - Publications
 
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Created: Tue, 31 May 2011, 19:37:16 EST by Assoc Prof Peter Thorn on behalf of Institute for Molecular Bioscience