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bioRxiv · 10.1101/255158

Two contractile pools of actomyosin distinctly load and tune 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.\n\nDuring 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.

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Kale, G. R., Yang, X., Philippe, J.-M., Mani, M., Lenne, P.-F., Lecuit, T.. 2018-01-27. Two contractile pools of actomyosin distinctly load and tune E-cadherin levels during morphogenesis. https://doi.org/10.1101/255158

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