Choi W, Acharya BR, Peyret G, Fardin MA, Mège RM, Ladoux B, Yap AS, Fanning AS, Peifer M (2016)
Publication Type: Journal article
Publication year: 2016
Book Volume: 213
Pages Range: 243-260
Journal Issue: 2
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.
APA:
Choi, W., Acharya, B.R., Peyret, G., Fardin, M.A., Mège, R.M., Ladoux, B.,... Peifer, M. (2016). Remodeling the zonula adherens in response to tension and the role of afadin in this response. The Journal of Cell Biology, 213(2), 243-260. https://doi.org/10.1083/jcb.201506115
MLA:
Choi, Wangsun, et al. "Remodeling the zonula adherens in response to tension and the role of afadin in this response." The Journal of Cell Biology 213.2 (2016): 243-260.
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