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J Cell Biol. 2017 Sep 4;216(9):2959-2977. doi: 10.1083/jcb.201611117. Epub 2017 Jul 7.

Membrane tension controls adhesion positioning at the leading edge of cells.

Author information

1
Mechanobiology Institute, National University of Singapore, Singapore.
2
Laboratório de Pinças Óticas, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
3
Institute FIRC (Italian Foundation for Cancer Research) of Molecular Oncology (IFOM-FIRC), Milan, Italy.
4
Institute for Bioengineering of Catalonia, The Barcelona Institute of Science and Technology, Barcelona, Spain.
5
Centre National de la Recherche Scientifique, École Supérieure de Physique et de Chimie Industrielles Paristech, Paris, France.
6
University of Barcelona, Barcelona, Spain.
7
Centre for Computational Biology, Duke-National University of Singapore Graduate Medical School, Singapore.
8
Mechanobiology Institute, National University of Singapore, Singapore nils.gauthier@ifom.eu.

Abstract

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.

PMID:
28687667
PMCID:
PMC5584154
DOI:
10.1083/jcb.201611117
[Indexed for MEDLINE]
Free PMC Article

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