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First published online 22 November 2005
doi: 10.1242/jcs.02700

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Hyper-adhesion in desmosomes: its regulation in wound healing and possible relationship to cadherin crystal structure

David R. Garrod, Mohamed Y. Berika^*, William F. Bardsley, David Holmes and Lydia Tabernero

Faculty of Life Sciences, Michael Smith Building, Oxford Road, University of Manchester, Manchester, M13 9PT, UK

Author for correspondence (e-mail: lydia.tabernero{at}manchester.ac.uk)

Accepted 9 September 2005

The resistance of tissues to physical stress is dependent upon strong cell-cell adhesion in which desmosomes play a crucial role. We propose that desmosomes fulfil this function by adopting a more strongly adhesive state, hyper-adhesion, than other junctions. We show that the hyper-adhesive desmosomes in epidermis resist disruption by ethylene glycol bis(2-aminoethyl ether)-N,N,N'N'-tetraacetic acid (EGTA) and are thus independent of Ca²⁺. We propose that Ca²⁺ independence is the normal condition for tissue desmosomes. Ca²⁺ independence is associated with an organised arrangement of the intercellular adhesive material exemplified by a dense midline. When epidermis is wounded, desmosomes in the wound-edge epithelium lose hyper-adhesiveness and become Ca²⁺ dependent, i.e. readily dissociated by EGTA. Ca²⁺-dependent desmosomes lack a midline and show narrowing of the intercellular space. We suggest that this indicates a less-organised, weakly adhesive arrangement of the desmosomal cadherins, resembling classical cadherins in adherens junctions. Transition to Ca²⁺ dependence on wounding is accompanied by relocalisation of protein kinase C to desmosomal plaques suggesting that an `inside-out' transmembrane signal is responsible for changing desmosomal adhesiveness. We model hyper-adhesive desmosomes using the crystal packing observed for the ectodomain of C-cadherin and show how the regularity of this 3D array provides a possible explanation for Ca²⁺ independence.

Key words: Desmosome, Cadherin, Cell-cell adhesion, Wound healing, Protein kinase C

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