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Nat Cell Biol. 2014 Jun;16(6):587-94. doi: 10.1038/ncb2973. Epub 2014 May 25.

Actin dynamics modulate mechanosensitive immobilization of E-cadherin at adherens junctions.

Author information

1
Mechanobiology Institute, National University of Singapore, 5A Engineering Drive 1, Singapore 117411, Singapore.
2
Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, Singapore 117596, Singapore.
3
1] Mechanobiology Institute, National University of Singapore, 5A Engineering Drive 1, Singapore 117411, Singapore [2] Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, Singapore 117596, Singapore [3] Institute of Molecular Cell Biology, A*STAR, 61 Biopolis Drive, Singapore 138673, Singapore [4].
4
1] Mechanobiology Institute, National University of Singapore, 5A Engineering Drive 1, Singapore 117411, Singapore [2].

Abstract

Mechanical stress is increasingly being shown to be a potent modulator of cell-cell junctional morphologies in developmental and homeostatic processes. Intercellular force sensing is thus expected to be an important regulator of cell signalling and tissue integrity. In particular, the interplay between myosin contractility, actin dynamics and E-cadherin recruitment largely remains to be uncovered. We devised a suspended cell doublet assay to quantitatively assess the correlation between myosin II activity and local E-cadherin recruitment. The single junction of the doublet exhibited a stereotypical morphology, with E-cadherin accumulating into clusters of varied concentrations at the rim of the circular contact. This local recruitment into clusters derived from the sequestration of E-cadherin through a myosin-II-driven modulation of actin turnover. We exemplify how the regulation of actin dynamics provides a mechanism for the mechanosensitive response of cell contacts.

PMID:
24859003
DOI:
10.1038/ncb2973
[Indexed for MEDLINE]

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