Distinct contributions of tensile and shear stress on E-cadherin levels during morphogenesis

Girish R. Kale, Xingbo Yang, Jean-Marc Philippe, Madhav Mani, Pierre-François Lenne () and Thomas Lecuit ()
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Girish R. Kale: Aix Marseille Université, CNRS, IBDM-UMR7288, Turing Center for Living Systems
Xingbo Yang: Northwestern University
Jean-Marc Philippe: Aix Marseille Université, CNRS, IBDM-UMR7288, Turing Center for Living Systems
Madhav Mani: Northwestern University
Pierre-François Lenne: Aix Marseille Université, CNRS, IBDM-UMR7288, Turing Center for Living Systems
Thomas Lecuit: Aix Marseille Université, CNRS, IBDM-UMR7288, Turing Center for Living Systems

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract During epithelial morphogenesis, cell contacts (junctions) are constantly remodeled by mechanical forces that work against adhesive forces. E-cadherin complexes play a pivotal role in this process by providing persistent cell adhesion and by transmitting mechanical tension. In this context, it is unclear how mechanical forces affect E-cadherin adhesion and junction dynamics. During Drosophila embryo axis elongation, Myosin-II activity in the apico-medial and junctional cortex generates mechanical forces to drive junction remodeling. Here we report that the ratio between Vinculin and E-cadherin intensities acts as a ratiometric readout for these mechanical forces (load) at E-cadherin complexes. Medial Myosin-II loads E-cadherin complexes on all junctions, exerts tensile forces, and increases levels of E-cadherin. Junctional Myosin-II, on the other hand, biases the distribution of load between junctions of the same cell, exerts shear forces, and decreases the levels of E-cadherin. This work suggests distinct effects of tensile versus shear stresses on E-cadherin adhesion.

Date: 2018
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DOI: 10.1038/s41467-018-07448-8

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