Frustrated endocytosis controls contractility-independent mechanotransduction at clathrin-coated structures.
Nat Commun
; 9(1): 3825, 2018 09 20.
Article
em En
| MEDLINE
| ID: mdl-30237420
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 αvß5 integrin, and is a consequence of frustrated endocytosis whereby αvß5 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Vesículas Revestidas por Clatrina
/
Mecanotransdução Celular
/
Endocitose
Limite:
Humans
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article