Even though the functions of adherens junctions (AJ) across multiple length scales, spanning from molecular to tissue levels are well understood, the processes including how mechanical force transmissions are mediated and regulated through AJ remain unclear.
In this study, with the use of iPALM superresolution microscopy, it is confirmed that alpha-catenin depletion induces vinculin disengagement from the cadherin/catenin layer.
Fig. 4 | Junctional tension and stability are supported by activated vinculin interaction withβ-catenin when α-catenin is depleted. (c) Representative time-lapse montages of recoil upon laser ablation. Edges of junction are denoted by red dots. Scale bar, 10um. (d) Trajectory of junctional recoil following ablation. (e) Plot of initial recoil rate after laser ablation for the indicated conditions.
Despite the significant depletion of alpha-catenin, vinculin could still localize at cadherin-mediated adhesions (Fig. 2b) to form a physical connection between the cadherin-catenin compartment and the actin cytoskeleton.
Fig. 2b | Localisation of vinculin constructs to AJs in MDCK wt and MDCK alpha-catenin KD in monolayer. Maximum intensity projection of vinculin (GFP, green channel) and E-cadherin (antibody probes, red channel), and merged image.
In conclusion, understanding how proteins of the adhesive complex self-organise and integrate into functional higher-order machineries that allow cells to aggregate into mechanically resistant and highly dynamic tissues, is the first step to provide mechanistic understanding of the mechanical basis for development and cancer transformation.
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