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. Author manuscript; available in PMC: 2012 Jun 6.
Published in final edited form as: Biochem Soc Trans. 2008 Apr;36(Pt 2):149–155. doi: 10.1042/BST0360149

Figure 3. A model for propagation of cell–cell adhesion in which two zones of Rho family GTPase activity are restricted to the edges of the cell–cell contact as it expands laterally.

Figure 3

Left: cell–cell adhesion between pairs of MDCK cells involves initial E-cadherin engagement, followed by propagation and finally compaction of the contact. Upper-right: the initial zone comprises a zone of cadherin engagement (orange); a zone of active Rac1 and its downstream effectors, the Arp2/3 complex and lamellipodia, localized to de novo contacts between cells at the edges of the zone of cadherin engagement (blue); and the zone of RhoA and its downstream effector actomyosin contractility, restricted to the edges of the contact and is required to drive expansion and completion of cell–cell adhesion (green). The activity zone of Rac1 is transient and rapidly diminishes as cadherin accumulates, but a new round of activation occurs at the periphery of the contacting membranes that would push the membranes together to initiate new E-cadherin adhesion. These sequential signalling zones comprising E-cadherin accumulation, Rac1-induced lamellipodia and RhoA-induced actomyosin contraction co-ordinate the induction, propagation and expansion of the cell–cell contact. Lower-right: a model representing regulatory interactions between cadherin, p120-catenin, Rho GTPases and integrins (-, negative regulation; +, positive regulation) (see the text for details).