Frustrated endocytosis controls contractility-independent mechanotransduction at clathrin-coated structures
2018 | journal article; research paper
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Frustrated endocytosis controls contractility-independent mechanotransduction at clathrin-coated structures
Baschieri, F.; Dayot, S.; Elkhatib, N.; Ly, N.; Capmany, A.; Schauer, K. & Betz, T. et al. (2018)
Nature Communications, 9(1) pp. 3825. DOI: https://doi.org/10.1038/s41467-018-06367-y
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- Authors
- Baschieri, Francesco; Dayot, Stéphane; Elkhatib, Nadia; Ly, Nathalie; Capmany, Anahi; Schauer, Kristine; Betz, Timo ; Vignjevic, Danijela Matic; Poincloux, Renaud; Montagnac, Guillaume
- 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.
- Issue Date
- 2018
- Journal
- Nature Communications
- ISSN
- 2041-1723
- Language
- English