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Titolo:
Different effects of dominant negative mutants of desmocollin and desmoglein on the cell-cell adhesion of keratinocytes
Autore:
Hanakawa, Y; Amagai, M; Shirakata, Y; Sayama, K; Hashimoto, K;
Indirizzi:
Ehime Univ, Sch Med, Dept Dermatol, Matsuyama, Ehime 790, Japan Ehime Univ Matsuyama Ehime Japan 790 ermatol, Matsuyama, Ehime 790, Japan Keio Univ, Sch Med, Dept Dermatol, Tokyo, Japan Keio Univ Tokyo JapanKeio Univ, Sch Med, Dept Dermatol, Tokyo, Japan
Titolo Testata:
JOURNAL OF CELL SCIENCE
fascicolo: 10, volume: 113, anno: 2000,
pagine: 1803 - 1811
SICI:
0021-9533(200005)113:10<1803:DEODNM>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERMEDIATE FILAMENT ANCHORAGE; DESMOSOMAL CADHERINS; PEMPHIGUS-VULGARIS; EPITHELIAL-CELLS; CATENIN COMPLEX; FULL-LENGTH; PLAKOGLOBIN; COMPONENTS; ORGANIZATION; EXPRESSION;
Keywords:
desmosome; adherens junction; desmocollin; desmoglein; E-cadherin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Hanakawa, Y Ehime Univ, Sch Med, Dept Dermatol, Matsuyama, Ehime 790, Japan Ehime Univ Matsuyama Ehime Japan 790 suyama, Ehime 790, Japan
Citazione:
Y. Hanakawa et al., "Different effects of dominant negative mutants of desmocollin and desmoglein on the cell-cell adhesion of keratinocytes", J CELL SCI, 113(10), 2000, pp. 1803-1811

Abstract

Desmosomes contain two types of cadherin: desmocollin (Dsc) and desmoglein(Dsg). In this study, we examined the different roles that Dsc and Dsg play in the formation of desmosomes, by using dominant-negative mutants. We constructed recombinant adenoviruses (Ad) containing truncated mutants of E-cadherin, desmocollin 3a, and desmoglein 3 lacking a large part of their extracellular domains (Ecad Delta EC, Dsc3s Delta EC, Dsg3 Delta EC), using the Cre-loxP Ad system to circumvent the problem of the toxicity of the mutants to virus-producing cells. When Dsc3a Delta EC Ad-infected HaCaT cells were cultured with high levels of calcium, E-cadherin and beta-catenin, whichare marker molecules for the adherens junction, disappeared from the cell-cell contact sites, and cell-cell adhesion was disrupted. This also occurred in the cells infected with Ecad Delta EC Ad. With Dsg3 Delta EC Ad infection, keratin insertion at the cell-cell contact sites was inhibited and desmoplakin, a marker of desmosomes, was stained in perinuclear dots while theadherens junctions remained intact. Dsc3a Delta EC Ad inhibited the induction of adherens junctions and the subsequent formation of desmosomes with the calcium shift, while Dsg3 Delta EC Ad only inhibited the formation of desmosomes. To further determine whether Dsc3s Delta EC directly affected adherens junctions, mouse fibroblast L cells transfected,vith E-cadherin (LEC5) were infected with these mutant Ads. Both Ds3a Delta EC and Ecad Delta ECinhibited the cell-cell adhesion of LEGS cells, as determined by the cell aggregation assay, while Dsg3 Delta EC did not. These results indicate thatthe dominant negative effects of Dsg3 Delta EC were restricted to desmosomes, while those of Dsc3a Delta EC were observed in both desmosomes and adherens junctions. Furthermore, the cytoplasmic domain of Dsc3a Delta EC coprecipitated both plakoglobin and beta-catenin in HaCaT cells. In addition, beta-catenin was found to bind the endogenous Dsc in HaCaT cells. These findings lead us to speculate that Dsc interacts with components of the adherensjunctions through beta-catenin, and plays a role in nucleating desmosomes after the adherens junctions have been established.

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Documento generato il 29/09/20 alle ore 23:53:33