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Article Dans Une Revue Journal of Cell Biology Année : 2016

Remodeling the zonula adherens in response to tension and the role of afadin in this response.

Résumé

Morphogenesis requires dynamic coordination between cell-cell adhesion and the cytoskeleton to allow cells to change shape and move without losing tissue integrity. We used genetic tools and superresolution microscopy in a simple model epithelial cell line to define how the molecular architecture of cell-cell zonula adherens (ZA) is modified in response to elevated contractility, and how these cells maintain tissue integrity. We previously found that depleting zonula occludens 1 (ZO-1) family proteins in MDCK cells induces a highly organized contractile actomyosin array at the ZA. We find that ZO knockdown elevates contractility via a Shroom3/Rho-associated, coiled-coil containing protein kinase (ROCK) pathway. Our data suggest that each bicellular border is an independent contractile unit, with actin cables anchored end-on to cadherin complexes at tricellular junctions. Cells respond to elevated contractility by increasing junctional afadin. Although ZO/afadin knockdown did not prevent contractile array assembly, it dramatically altered cell shape and barrier function in response to elevated contractility. We propose that afadin acts as a robust protein scaffold that maintains ZA architecture at tricellular junctions.

Dates et versions

hal-01323924 , version 1 (31-05-2016)

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Citer

Wangsun Choi, Bipul R Acharya, Grégoire Peyret, Marc-Antoine Fardin, René-Marc Mège, et al.. Remodeling the zonula adherens in response to tension and the role of afadin in this response.. Journal of Cell Biology, 2016, 213 (2), pp.243-60. ⟨10.1083/jcb.201506115⟩. ⟨hal-01323924⟩
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