The Motor Protein Myosin-X Transports VE-Cadherin along Filopodia To Allow the Formation of Early Endothelial Cell-Cell Contacts▿ †
Autor: | Camille Maillefaud, Jean Patrick Schaal, Elizabeth A. Hewat, Mathilde Dubois, Adeline Chervin-Pétinot, Claire Durmort, Stéphanie Heyraud, Olivier Lambert, Danielle Gulino-Debrac, Philippe Huber, Sébastien Almagro |
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Jazyk: | angličtina |
Rok vydání: | 2010 |
Předmět: |
Recombinant Fusion Proteins
Arp2/3 complex macromolecular substances Myosins Motor protein 03 medical and health sciences 0302 clinical medicine Antigens CD Myosin Humans Pseudopodia Molecular Biology Cells Cultured 030304 developmental biology 0303 health sciences biology Cryoelectron Microscopy Endothelial Cells Catenins Cell Biology Articles Actin cytoskeleton Cadherins Cell biology Protein Structure Tertiary Intercellular Junctions Fimbrin Paracytophagy biology.protein Filopodia 030217 neurology & neurosurgery |
Popis: | Vascular endothelium (VE), the monolayer of endothelial cells that lines the vascular tree, undergoes damage at the basis of some vascular diseases. Its integrity is maintained by VE-cadherin, an adhesive receptor localized at cell-cell junctions. Here, we show that VE-cadherin is also located at the tip and along filopodia in sparse or subconfluent endothelial cells. We observed that VE-cadherin navigates along intrafilopodial actin filaments. We found that the actin motor protein myosin-X is colocalized and moves synchronously with filopodial VE-cadherin. Immunoprecipitation and pulldown assays confirmed that myosin-X is directly associated with the VE-cadherin complex. Furthermore, expression of a dominant-negative mutant of myosin-X revealed that myosin-X is required for VE-cadherin export to cell edges and filopodia. These features indicate that myosin-X establishes a link between the actin cytoskeleton and VE-cadherin, thereby allowing VE-cadherin transportation along intrafilopodial actin cables. In conclusion, we propose that VE-cadherin trafficking along filopodia using myosin-X motor protein is a prerequisite for cell-cell junction formation. This mechanism may have functional consequences for endothelium repair in pathological settings. |
Databáze: | OpenAIRE |
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