Targeted deletion of the sciellin gene resulted in normal development and maturation
Corresponding Author
Howard P. Baden
Department of Dermatology, Cutaneous Biology Research Center, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts
Massachusetts General Hospital, Cutaneous Biology Research Center, 13th Street Building 149, Charlestown MA 02129Search for more papers by this authorMarie-France Champliaud
Laboratoire de Physiopathologie Cellulaire et Moleculaire de la Retine, Universite Louis Pasteur, Strasbourg, France
Search for more papers by this authorAlain Viel
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts
Search for more papers by this authorCorresponding Author
Howard P. Baden
Department of Dermatology, Cutaneous Biology Research Center, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts
Massachusetts General Hospital, Cutaneous Biology Research Center, 13th Street Building 149, Charlestown MA 02129Search for more papers by this authorMarie-France Champliaud
Laboratoire de Physiopathologie Cellulaire et Moleculaire de la Retine, Universite Louis Pasteur, Strasbourg, France
Search for more papers by this authorAlain Viel
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts
Search for more papers by this authorAbstract
Sciellin, together with other precursor proteins, was cross-linked by transglutaminase 1 to form the cornified envelope, an essential component of the physical barrier of the epidermis and stratified squamous epithelia. To more fully understand the function of sciellin in cornified envelope formation, we generated sciellin null mice. The mice appeared normal in their development and maturation and there were no structural features that distinguished them from littermate controls. Isolated cornified envelopes appeared normal in structure and were not more fragile to mechanical stress. There was no evidence of decreased barrier function or altered expression of other cornified envelope components. Transgenic mice expressing the repeat domain appeared to have a normal phenotype, like the null, and did not alter endogenous sciellin expression. We conclude that sciellin null mice had no structural anomalies and the transgenic mice did not act as a dominant-negative mutation. genesis 42:219–228, 2005. © 2005 Wiley-Liss, Inc.
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