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Distinct contributions of tensile and shear stress on E-cadherin levels during morphogenesis
Epithelial tissues are highly dynamic. During embryonic morphogenesis cell contacts are constantly remodeled. This stems from active contractile forces that work against adhesive forces at cell interfaces. E-cadherin complexes play a pivotal role in this process as they both support inter-molecular adhesive forces and transmit mechanical tension due to their coupling to the cortical contractile actomyosin networks. In this context, it is unclear how tensile forces affect E-cadherin adhesion complexes and junction dynamics. Addressing this calls for methods to estimate the tensile forces (load) experienced by adhesion complexes themselves. We address this during the early morphogenesis of the Drosophila embryonic ectoderm. Tensile forces generated by Myosin-II in the apico-medial cortex (medial Myosin-II) and in the junctional cortex (junctional Myosin-II) are responsible for junction remodeling. We combined mechanical inference and laser ablations to map tension at cell junctions. We also established the ratio between Vinculin and E-cadherin intensities as a ratiometric readout that measures the load at adhesion complexes. Combining these tools, we show that the tension generated in both medial and junction pools of Myosin-II imposes load on E-cadherin adhesion complexes. Medial Myosin-II loads adhesion complexes on all junctions of a cell and increases levels of E-cadherin. Junctional Myosin-II, on the other hand, biases the distribution of the load between junctions of the same cell and exerts shear forces, which decrease the levels of E-cadherin. This work highlights the difference between medial Myosin-II and junctional Myosin-II in regulating E-cadherin levels during junction remodeling and suggests distinct effects of shear versus tensile stresses on E-cadherin complexes and on the dynamics of adhesive cell contacts.
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