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

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Baschieri F,Dayot S,Elkhatib N,Ly N,Capmany A,Schauer K,Betz T,Vignjevic DM,Poincloux R,Montagnac G

doi

10.1038/s41467-018-06367-y

subject

Has Abstract

pub_date

2018-09-20 00:00:00

pages

3825

issue

1

issn

2041-1723

pii

10.1038/s41467-018-06367-y

journal_volume

9

pub_type

杂志文章

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