Frustrated endocytosis controls contractility-independent mechanotransduction at clathrin-coated structures

Francesco Baschieri (), Stéphane Dayot, Nadia Elkhatib, Nathalie Ly, Anahi Capmany, Kristine Schauer, Timo Betz, Danijela Matic Vignjevic, Renaud Poincloux and Guillaume Montagnac ()
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Francesco Baschieri: Université Paris-Saclay
Stéphane Dayot: Université Paris-Saclay
Nadia Elkhatib: Université Paris-Saclay
Nathalie Ly: Université Paris-Saclay
Anahi Capmany: Centre Universitaire
Kristine Schauer: Centre Universitaire
Timo Betz: University of Münster
Danijela Matic Vignjevic: Centre Universitaire
Renaud Poincloux: UPS
Guillaume Montagnac: Université Paris-Saclay

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract It is generally assumed that cells interrogate the mechanical properties of their environment by pushing and pulling on the extracellular matrix (ECM). For instance, acto-myosin-dependent contraction forces exerted at focal adhesions (FAs) allow the cell to actively probe substrate elasticity. Here, we report that a subset of long-lived and flat clathrin-coated structures (CCSs), also termed plaques, are contractility-independent mechanosensitive signaling platforms. We observed that plaques assemble in response to increasing substrate rigidity and that this is independent of FAs, actin and myosin-II activity. We show that plaque assembly depends on αvβ5 integrin, and is a consequence of frustrated endocytosis whereby αvβ5 tightly engaged with the stiff substrate locally stalls CCS dynamics. We also report that plaques serve as platforms for receptor-dependent signaling and are required for increased Erk activation and cell proliferation on stiff environments. We conclude that CCSs are mechanotransduction structures that sense substrate rigidity independently of cell contractility.

Date: 2018
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DOI: 10.1038/s41467-018-06367-y

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