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First published online August 20, 2008

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Desmocollin 3 holds it together...

Desmosomes are cell-cell junctions that maintain tissue stability, particularly in skin, heart and other tissues that undergo substantial mechanical stress; consequently, defects in desmosomal adhesion cause several tissue-fragility disorders. The desmocollins (DSC1-DSC3) are key components of desmosomes, but their precise biological function has not been well understood. Now, Peter Koch and colleagues (p. 2844) explore the role of DSC3 in cell-cell adhesion. The authors previously showed that Dsc3-null mice have an embryonic-lethal phenotype; they now describe the generation of epidermis-specific Dsc3 conditional-knockout mice. Some of the mutant mice, they show, have large intra-epidermal blisters at birth, and all adult mice exhibit severe skin lesions. Moreover, cell sheets that are generated from mutant keratinocytes in vitro are considerably less resistant to stress than wild-type sheets. In addition, the two epidermal-cell layers that anchor telogen club hairs do not adhere correctly in the absence of DSC3; consequently, mutant mice exhibit telogen hair loss. Importantly, the lesions that are observed in individuals with the skin-blistering disease pemphigus vulgaris are histologically indistinguishable from those of the mutant mice. The authors conclude, therefore, that impaired DSC3 activity might promote pemphigus-vulgaris-like diseases.

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Related articles in JCS:

Loss of desmocollin 3 in mice leads to epidermal blistering

Jiangli Chen, Zhining Den, and Peter J. Koch
JCS 2008 121: 2844-2849. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?