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J. Biol. Chem., Vol. 279, Issue 49, 51524-51533, December 3, 2004

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Krtap16, Characterization of a New Hair Keratin-associated Protein (KAP) Gene Complex on Mouse Chromosome 16 and Evidence for Regulation by Hoxc13^*

Nathanael D. Pruett, Tatiana V. Tkatchenko, Luis Jave-Suarez, Donna F. Jacobs, Christopher S. Potter, Andrei V. Tkatchenko, Jürgen Schweizer, and Alexander Awgulewitsch¶||

From the Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, the Section of Normal and Neoplastic Epidermal Differentiation, German Cancer Research Center, 69120 Heidelberg, Germany, and the ^¶Department of Dermatology, Medical University of South Carolina, Charleston, South Carolina 29425

Intermediate filament (IF) keratins and keratin-associated proteins (KAPs) are principal structural components of hair and encoded by members of multiple gene families. The severe hair growth defects observed upon aberrant expression of certain keratin and KAP genes in both mouse and man suggest that proper hair growth requires their spatio-temporally coordinated activation. An essential prerequisite for studying these cis-regulatory mechanisms is to define corresponding gene families, their genomic organization, and expression patterns. This work characterizes eight recently identified high glycine/tyrosine (HGT)-type KAP genes collectively designated Krtap16-n. These genes are shown to be integrated into a larger KAP gene domain on mouse chromosome 16 (MMU16) that is orthologous to a recently described HGT- and high sulfur (HS)-type KAP gene complex on human chromosome 21q22.11. All Krtap16 genes exhibit strong expression in a narrowly defined pattern restricted to the lower and middle cortical region of the hair shaft in both developing and cycling hair. During hair follicle regression (catagen), expression levels decrease until expression is no longer detectable in follicles at resting stage (telogen). Since isolation of the Krtap16 genes was based on their differential expression in transgenic mice overexpressing the Hoxc13 transcriptional regulator in hair, we examined whether bona fide Hoxc13 binding sites associated with these genes might be functionally relevant by performing electrophoretic mobility shift assays (EMSAs). The data provide evidence for sequence-specific interaction between Hoxc13 and Krtap16 genes, thus supporting the concept of a regulatory relationship between Hoxc13 and these KAP genes.

Received for publication, April 19, 2004 , and in revised form, September 21, 2004.

^* This work was supported by Grant AR47204 from the National Institutes of Health and in part by Medical University of South Carolina Institutional Research Funds of 2004-05. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^|| To whom correspondence should be addressed: Dept. of Medicine, Medical University of South Carolina, 96 Jonathan Lucas St./Suite CSB 912, Charleston SC 29425. Tel.: 843-792-8946; Fax: 843-792-7121; E-mail: awgulewa{at}musc.edu.

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