Membrane tension controls adhesion positioning at the leading edge of cells

Cell migration is dependent on adhesion dynamics and actin cytoskeleton remodeling at the leading edge. These events may be physically constrained by the plasma membrane. Here, we show that the mechanical signal produced by an increase in plasma membrane tension triggers the positioning of new rows...

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Detalhes bibliográficos
Autores: Pontes, Bruno, Monzo, Pascale, Gole, Laurent, Le Roux, Anabel-Lise, Kosmalska, Anita Joanna, Tam, Zhi Yang, Luo, Weiwei, Kan, Sophie, Viasnoff, Virgile, Roca-Cusachs Soulere, Pere, Tucker-Kellogg, Lisa, Gauthier, Nils C.
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:España
Recursos:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/123547
Acesso em linha:https://hdl.handle.net/2445/123547
Access Level:acceso abierto
Palavra-chave:Membranes cel·lulars
Proteïnes citosquelètiques
Motilitat cel·lular
Migració cel·lular
Fisiologia animal
Genètica
Cell membranes
Cytoskeletal proteins
Cell motility
Cell migration
Animal physiology
Genetics
Descrição
Resumo:Cell migration is dependent on adhesion dynamics and actin cytoskeleton remodeling at the leading edge. These events may be physically constrained by the plasma membrane. Here, we show that the mechanical signal produced by an increase in plasma membrane tension triggers the positioning of new rows of adhesions at the leading edge. During protrusion, as membrane tension increases, velocity slows, and the lamellipodium buckles upward in a myosin II-independent manner. The buckling occurs between the front of the lamellipodium, where nascent adhesions are positioned in rows, and the base of the lamellipodium, where a vinculin-dependent clutch couples actin to previously positioned adhesions. As membrane tension decreases, protrusion resumes and buckling disappears, until the next cycle. We propose that the mechanical signal of membrane tension exerts upstream control in mechanotransduction by periodically compressing and relaxing the lamellipodium, leading to the positioning of adhesions at the leading edge of cells.