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Two contractile pools of actomyosin distinctly load and tune E-cadherin levels during morphogenesis

Girish R. Kale, Xingbo Yang, Jean-Marc Philippe, Madhav Mani, Pierre-François Lenne, Thomas Lecuit
doi: https://doi.org/10.1101/255158
Girish R. Kale
1Aix Marseille Université, CNRS, IBDM - UMR7288, 13009 Marseille, France.
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Xingbo Yang
2Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
3Northwestern University, 2145 Sheridan Road, Evanston, IL 60208, USA.
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Jean-Marc Philippe
1Aix Marseille Université, CNRS, IBDM - UMR7288, 13009 Marseille, France.
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Madhav Mani
3Northwestern University, 2145 Sheridan Road, Evanston, IL 60208, USA.
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Pierre-François Lenne
1Aix Marseille Université, CNRS, IBDM - UMR7288, 13009 Marseille, France.
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Thomas Lecuit
1Aix Marseille Université, CNRS, IBDM - UMR7288, 13009 Marseille, France.
4Collège de France, 11 Place Marcelin Berthelot, 75005 Paris, France.
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Abstract

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 Vinculin as a force sensor whose enrichment with respect to E-cadherin measures the load on adhesion complexes within each junction. 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 uniformly 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 correspond to a decrease in 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 suggest opposite effects of shear versus tensile stresses on E-cadherin complexes and on the dynamics of adhesive cell contacts.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted January 28, 2018.
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Two contractile pools of actomyosin distinctly load and tune E-cadherin levels during morphogenesis
Girish R. Kale, Xingbo Yang, Jean-Marc Philippe, Madhav Mani, Pierre-François Lenne, Thomas Lecuit
bioRxiv 255158; doi: https://doi.org/10.1101/255158
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Two contractile pools of actomyosin distinctly load and tune E-cadherin levels during morphogenesis
Girish R. Kale, Xingbo Yang, Jean-Marc Philippe, Madhav Mani, Pierre-François Lenne, Thomas Lecuit
bioRxiv 255158; doi: https://doi.org/10.1101/255158

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