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E-cadherin endocytosis is modulated by p120-catenin through the opposing actions of RhoA and Arf1

View ORCID ProfileJoshua Greig, View ORCID ProfileNatalia A. Bulgakova
doi: https://doi.org/10.1101/477760
Joshua Greig
1Department of Biomedical Science and Bateson Centre, The University of Sheffield, Sheffield S10 2TN, United Kingdom
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Natalia A. Bulgakova
1Department of Biomedical Science and Bateson Centre, The University of Sheffield, Sheffield S10 2TN, United Kingdom
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  • For correspondence: n.bulgakova@sheffield.ac.uk
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Abstract

The regulation of E-cadherin at the plasma membrane by endocytosis is of vital importance for developmental and disease. p120-catenin, which binds to the E-cadherin C-terminus, can both promote and inhibit E-cadherin endocytosis. However, little is known about what determines the directionality of p120-catenin activity, and the molecules downstream. Here, we have discovered that p120-catenin fine-tunes the clathrin-mediated endocytosis of E-cadherin in Drosophila embryonic epidermal cells. It simultaneously activated two actin-remodelling pathways with opposing effects: RhoA, which stabilized E-cadherin at the membrane, and Arf1, which promoted internalization. Epistasis experiments revealed that RhoA additionally inhibited Arf1. E-cadherin was efficiently endocytosed only in the presence of intermediate p120-catenin amounts with too little and too much p120-catenin inhibiting E-cadherin endocytosis. Finally, we found that p120-catenin levels altered the tension of the plasma membrane. Altogether, this shows that p120-catenin is a central hub which co-ordinates cell adhesion, endocytosis, and actin dynamics with tissue tension.

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Posted January 26, 2019.
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E-cadherin endocytosis is modulated by p120-catenin through the opposing actions of RhoA and Arf1
Joshua Greig, Natalia A. Bulgakova
bioRxiv 477760; doi: https://doi.org/10.1101/477760
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E-cadherin endocytosis is modulated by p120-catenin through the opposing actions of RhoA and Arf1
Joshua Greig, Natalia A. Bulgakova
bioRxiv 477760; doi: https://doi.org/10.1101/477760

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