Abstract

Cell–cell adhesion is fundamental to the formation of tissues and organs. Accumulating evidence indicates that cell–cell adhesion is not a static process, but it actively controls social cell behavior. For example, in developing epithelial layers, local constriction of cell–cell junctions autonomously induces the intercalation of cells, a process required for the convergent–extension of tissues. The junctional constriction also plays a role in the folding of epithelial layers, which is important for many types of epithelial morphogenesis, such as neural tube formation. On the other hand, loosening of cell–cell contacts is known to assist cell migration as seen in cancer invasion. How do the cells regulate their contacts with others? Cadherin is the major cell–cell adhesion receptor, which structurally builds “adherens junction (AJ)” at the apical cellular interfaces. In the AJs, cadherin interacts with a couple of cytoplasmic proteins, called catenins. Importantly, the cadherin–catenin complex is further linked with the cytoskeletal structures, such as F-actin and microtubules that are known to serve for regulating a number of cellular behaviors, such as cell motility and shaping. Thus, the adhesive and motile elements are combined into single machinery, and this explains why the cell junctions can have such dynamic and regulatable properties. We have been analyzing the molecular details of AJ–actin or microtubule interactions, and also their potential roles in epithelial or neural morphogenesis. I will overview our recent progresses in the studies of these problems.

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