Tyrosine dephosphorylated cortactin downregulates contractility at the epithelial zonula adherens through SRGAP1

Xuan Liang, Srikanth Budnar, Shafali Gupta, Suzie Verma, Siew-Ping Han, Michelle M. Hill, Roger J. Daly, Robert G. Parton, Nicholas A. Hamilton, Guillermo A. Gomez () and Alpha S. Yap ()
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Xuan Liang: Division of Cell Biology and Molecular Medicine, The University of Queensland
Srikanth Budnar: Division of Cell Biology and Molecular Medicine, The University of Queensland
Shafali Gupta: Division of Cell Biology and Molecular Medicine, The University of Queensland
Suzie Verma: Division of Cell Biology and Molecular Medicine, The University of Queensland
Siew-Ping Han: Division of Cell Biology and Molecular Medicine, The University of Queensland
Michelle M. Hill: The University of Queensland Diamantina Institute
Roger J. Daly: Monash University
Robert G. Parton: Division of Cell Biology and Molecular Medicine, The University of Queensland
Nicholas A. Hamilton: Division of Cell Biology and Molecular Medicine, The University of Queensland
Guillermo A. Gomez: Division of Cell Biology and Molecular Medicine, The University of Queensland
Alpha S. Yap: Division of Cell Biology and Molecular Medicine, The University of Queensland

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Contractile adherens junctions support cell−cell adhesion, epithelial integrity, and morphogenesis. Much effort has been devoted to understanding how contractility is established; however, less is known about whether contractility can be actively downregulated at junctions nor what function this might serve. We now identify such an inhibitory pathway that is mediated by the cytoskeletal scaffold, cortactin. Mutations of cortactin that prevent its tyrosine phosphorylation downregulate RhoA signaling and compromise the ability of epithelial cells to generate a contractile zonula adherens. This is mediated by the RhoA antagonist, SRGAP1. We further demonstrate that this mechanism is co-opted by hepatocyte growth factor to promote junctional relaxation and motility in epithelial collectives. Together, our findings identify a novel function of cortactin as a regulator of RhoA signaling that can be utilized by morphogenetic regulators for the active downregulation of junctional contractility.

Date: 2017
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DOI: 10.1038/s41467-017-00797-w

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