| First Author | Garrod DR | Year | 2005 |
| Journal | J Cell Sci | Volume | 118 |
| Issue | Pt 24 | Pages | 5743-54 |
| PubMed ID | 16303847 | Mgi Jnum | J:105610 |
| Mgi Id | MGI:3616116 | Doi | 10.1242/jcs.02700 |
| Citation | Garrod DR, et al. (2005) Hyper-adhesion in desmosomes: its regulation in wound healing and possible relationship to cadherin crystal structure. J Cell Sci 118(Pt 24):5743-54 |
| abstractText | 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 Ca(2+). We propose that Ca(2+) independence is the normal condition for tissue desmosomes. Ca(2+) 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 Ca(2+) dependent, i.e. readily dissociated by EGTA. Ca(2+)-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 Ca(2+) dependence on wounding is accompanied by relocalisation of protein kinase C alpha 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 Ca(2+) independence. |
