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First published online 5 August 2008
doi: 10.1242/jcs.031518

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Loss of desmocollin 3 in mice leads to epidermal blistering

¹ Department of Dermatology, Charles C. Gates Regenerative Medicine and Stem Cell Biology Program, University of Colorado Denver, Aurora, CO 80045, USA
² Department of Dermatology, Baylor College of Medicine, Houston, TX 77030, USA

^* Author for correspondence (e-mail: peter.koch{at}ucdenver.edu)

Accepted 9 June 2008

Desmocollin 3 (DSC3) belongs to a subfamily of cadherins and is a major component of desmosomes in keratinocytes of stratified epithelia, such as the epidermis. Based on its amino acid sequence homology to classical cadherins, such as E-cadherin, it has been postulated that DSC3 functions as a cell-adhesion molecule. To test this hypothesis, we assessed the function of DSC3 in the development and maintenance of stratified epithelia, in particular the epidermis and hair follicles. Using a conditional null allele, we show that loss of Dsc3 function in the epidermis causes impaired cell–cell adhesion, leading to intra-epidermal blistering and telogen hair loss. Furthermore, the lesions in Dsc3-null skin resemble those observed in individuals with pemphigus vulgaris (PV), indicating that impaired Dsc3 function could be a potential cause of PV-like inherited or acquired skin blistering diseases.

Key words: Desmosomes, Desmocollin 3, Skin fragility, Hair loss, Dsc3 null mice

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