Author/Authors :
Ana Kljuic، نويسنده , , Hisham Bazzi، نويسنده , , John P Sundberg، نويسنده , , Amalia Martinez-Mir، نويسنده , , Ryan OʹShaughnessy، نويسنده , , My G Mahoney، نويسنده , , Moise Levy، نويسنده , , Xavier Montagutelli، نويسنده , , Wasim Ahmad، نويسنده , , Vincent M Aita، نويسنده , , Derek Gordon، نويسنده , , Jouni Uitto، نويسنده , , David Whiting، نويسنده , , Jurg Ott، نويسنده , , Stuart Fischer، نويسنده , , T. Conrad Gilliam، نويسنده , , Colin AB Jahoda، نويسنده , , Rebecca J. Morris، نويسنده , , Andrei A Panteleyev، نويسنده , , Vu Thuong Nguyen، نويسنده , , et al.، نويسنده ,
Abstract :
Cell adhesion and communication are interdependent aspects of cell behavior that are critical for morphogenesis and tissue architecture. In the skin, epidermal adhesion is mediated in part by specialized cell-cell junctions known as desmosomes, which are characterized by the presence of desmosomal cadherins, known as desmogleins and desmocollins. We identified a cadherin family member, desmoglein 4, which is expressed in the suprabasal epidermis and hair follicle. The essential role of desmoglein 4 in skin was established by identifying mutations in families with inherited hypotrichosis, as well as in the lanceolate hair mouse. We also show that DSG4 is an autoantigen in pemphigus vulgaris. Characterization of the phenotype of naturally occurring mutant mice revealed disruption of desmosomal adhesion and perturbations in keratinocyte behavior. We provide evidence that desmoglein 4 is a key mediator of keratinocyte cell adhesion in the hair follicle, where it coordinates the transition from proliferation to differentiation.
