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

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Kale GR,Yang X,Philippe JM,Mani M,Lenne PF,Lecuit T

doi

10.1038/s41467-018-07448-8

subject

Has Abstract

pub_date

2018-11-27 00:00:00

pages

5021

issue

1

issn

2041-1723

pii

10.1038/s41467-018-07448-8

journal_volume

9

pub_type

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