Journal
BIOPHYSICAL JOURNAL
Volume 107, Issue 11, Pages 2652-2661Publisher
CELL PRESS
DOI: 10.1016/j.bpj.2014.10.045
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Funding
- National Health and Medical Research Council of Australia [1037320, 1044041, 1067405]
- Australian Research Council [DP120104667, FT130100659]
- Kids Cancer Project of the Oncology Research Foundation
- Australian Cancer Research Foundation
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The behavior of actomyosin critically determines morphologically distinct patterns of contractility found at the interface between adherent cells. One such pattern is found at the apical region (zonula adherens) of cell-cell junctions in epithelia, where clusters of the adhesion molecule E-cadherin concentrate in a static pattern. Meanwhile, E-cadherin clusters throughout lateral cell-cell contacts display dynamic movements in the plane of the junctions. To gain insight into the principles that determine the nature and organization of these dynamic structures, we analyze this behavior by modeling the 2D actomyosin cell cortex as an active fluid medium. The numerical simulations show that the stability of the actin filaments influences the spatial structure and dynamics of the system. We find that in addition to static Turing-type patterns, persistent dynamic behavior occurs in a wide range of parameters. In the 2D model, mechanical stress-dependent actin breakdown is shown to produce a continuously changing network of actin bridges, whereas with a constant breakdown rate, more isolated clusters of actomyosin tend to form. The model qualitatively reproduces the dynamic and stable patterns experimentally observed at the junctions between epithelial cells.
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