A reaction-diffusion model of the cadherin-catenin system

A possible mechanism for contact inhibition and implications for tumorigenesis

Journal Article (2010)
Author(s)

Markus Basan (Institut Curie Centre de Recherche)

Timon Idema (Universiteit Leiden)

Martin Lenz (Institut Curie Centre de Recherche)

Jean François Joanny (Institut Curie Centre de Recherche)

Thomas Risler (Institut Curie Centre de Recherche)

Affiliation
External organisation
DOI related publication
https://doi.org/10.1016/j.bpj.2010.03.051
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Publication Year
2010
Language
English
Affiliation
External organisation
Issue number
12
Volume number
98
Pages (from-to)
2770-2779

Abstract

Contact inhibition is the process by which cells switch from a motile growing state to a passive and stabilized state upon touching their neighbors. When two cells touch, an adhesion link is created between them by means of transmembrane E-cadherin proteins. Simultaneously, their actin filaments stop polymerizing in the direction perpendicular to the membrane and reorganize to create an apical belt that colocalizes with the adhesion links. Here, we propose a detailed quantitative model of the role of cytoplasmic β-catenin and a-catenin proteins in this process, treated as a reaction-diffusion system. Upon cell-cell contact the concentration in α-catenin dinners increases, inhibiting actin branching and thereby reducing cellular motility and expansion pressure. This model provides a mechanism for contact inhibition that could explain previously unrelated experimental findings on the role played by E-cadherin, β-catenin, and α-catenin in the cellular phenotype and in tumorigenesis. In particular, we address the effect of a knockout of the adenomatous polyposis coli tumor suppressor gene. Potential direct tests of our model are discussed.

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