Tension-sensitive actin assembly supports contractility at the epitherlial zonula adherens

Leerberg, Joanne M., Gomez, Guillermo A., Verma, Suzie, Moussa, Elliott J., Wu, Selwin K., Priya, Rashmi, Hoffman, Brenton D., Grashoff, Carsten, Schwartz, Martin A. and Yap, Alpha S. (2014) Tension-sensitive actin assembly supports contractility at the epitherlial zonula adherens. Current Biology, 24 15: 1689-1699. doi:10.1016/j.cub.2014.06.028


Author Leerberg, Joanne M.
Gomez, Guillermo A.
Verma, Suzie
Moussa, Elliott J.
Wu, Selwin K.
Priya, Rashmi
Hoffman, Brenton D.
Grashoff, Carsten
Schwartz, Martin A.
Yap, Alpha S.
Title Tension-sensitive actin assembly supports contractility at the epitherlial zonula adherens
Journal name Current Biology   Check publisher's open access policy
ISSN 0960-9822
1879-0445
Publication date 2014-08-04
Year available 2014
Sub-type Article (original research)
DOI 10.1016/j.cub.2014.06.028
Open Access Status
Volume 24
Issue 15
Start page 1689
End page 1699
Total pages 11
Place of publication Cambridge, MA United States
Publisher Cell Press
Collection year 2015
Language eng
Formatted abstract
Background
Actomyosin-based contractility acts on cadherin junctions to support tissue integrity and morphogenesis. The actomyosin apparatus of the epithelial zonula adherens (ZA) is built by coordinating junctional actin assembly with Myosin II activation. However, the physical interaction between Myosin and actin filaments that is necessary for contractility can induce actin filament turnover, potentially compromising the contractile apparatus itself.

Results
We now identify tension-sensitive actin assembly as one cellular solution to this design paradox. We show that junctional actin assembly is maintained by contractility in established junctions and increases when contractility is stimulated. The underlying mechanism entails the tension-sensitive recruitment of vinculin to the ZA. Vinculin, in turn, directly recruits Mena/VASP proteins to support junctional actin assembly. By combining strategies that uncouple Mena/VASP from vinculin or ectopically target Mena/VASP to junctions, we show that tension-sensitive actin assembly is necessary for junctional integrity and effective contractility at the ZA.

Conclusions
We conclude that tension-sensitive regulation of actin assembly represents a mechanism for epithelial cells to resolve potential design contradictions that are inherent in the way that the junctional actomyosin system is assembled. This emphasizes that maintenance and regulation of the actin scaffolds themselves influence how cells generate contractile tension.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
Institute for Molecular Bioscience - Publications
 
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Created: Thu, 14 Aug 2014, 11:59:15 EST by Susan Allen on behalf of Institute for Molecular Bioscience