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Lookup NU author(s): Dr Julia Reichelt
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Keratin K2 is one of the most abundant structural proteins of the epidermis; however, its biological significance has remained elusive. Here we show that suprabasal type II keratins, K1 and K2, are expressed in a mutually exclusive manner at different body sites of the mouse, with K2 being confined to the ear, sole, and tail skin. Deletion of K2 caused acanthosis and hyperkeratosis of the ear and the tail epidermis, corneocyte fragility, increased transepidermal water loss, and local inflammation in the ear skin. The loss of K2 was partially compensated by upregulation of K1 expression. However, a significant portion of K2-deficient suprabasal keratinocytes lacked a regular cytoskeleton and developed massive aggregates of the type I keratin, K10. Aggregate formation, but not hyperkeratosis, was suppressed by the deletion of both K2 and K10, whereas deletion of K10 alone caused clumping of K2 in ear skin. Taken together, this study demonstrates that K2 is a necessary and sufficient binding partner of K10 at distinct body sites of the mouse and that unbalanced expression of these keratins results in aggregate formation.
Author(s): Fischer H, Langbein L, Reichelt J, Praetzel-Wunder S, Buchberger M, Ghannadan M, Tschachler E, Eckhart L
Publication type: Article
Publication status: Published
Journal: Journal of Investigative Dermatology
Print publication date: 01/10/2014
Online publication date: 29/05/2014
Acceptance date: 02/04/2014
ISSN (print): 0022-202X
ISSN (electronic): 1523-1747
Publisher: Nature Publishing Group
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