Disease relevance of Hoxc13

• We show that transgenic mice overexpressing Hoxc13 in differentiating keratinocytes of hair follicles develop alopecia, accompanied by a progressive pathological skin condition that resembles ichthyosis [1].

High impact information on Hoxc13

• Hoxc13 is also expressed in vibrissae, in the filiform papillae of the tongue, and in hair follicles throughout the body; a pattern that apparently violates spatial colinearity [2].
• Since Hoxa1 is expressed early and Hoxc13 is expressed late in mouse embryogenesis, this study shows that single-copy GFP gene fusions can be used through most of mouse embryogenesis [3].
• Large-scale analysis of differential gene expression in postnatal skin of these mice identified 16 previously unknown and 13 known genes as presumptive Hoxc13 targets [1].
• Combined, these results provide a framework for understanding molecular mechanisms of Hoxc13 function in hair growth and development [1].
• We provide evidence that Foxq1 is a downstream target for Hoxc13 based on DNA binding studies as well as co-transfection and chromatin immunoprecipitation assays [4].

Biological context of Hoxc13

• We examine the Hoxc12 RNA expression pattern during both hair follicle morphogenesis and cycling in direct comparison to its only upstream neighbor, Hoxc13 [5].
• 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) [6].

Anatomical context of Hoxc13

• In addition to expression in the follicle, we detected Hoxc-13 in cells of the blood sinus surrounding vibrissal follicles and in scattered cells in the upper dermis of the skin [7].

Physical interactions of Hoxc13

• Transgenic mice overexpressing Hoxc13 in hair follicles (GC13 mice) exhibit complex phenotypic alterations including hair shaft defects and alopecia, as well as severe epidermal abnormalities [8].

Regulatory relationships of Hoxc13

• Epididymal cysteine-rich secretory protein 1 encoding gene is expressed in murine hair follicles and downregulated in mice overexpressing Hoxc13 [8].

Other interactions of Hoxc13

• Here, we show that the fluorescent signals produced by single-copy, targeted GFP in-frame fusions with two different murine Hox genes, Hoxa1 and Hoxc13, are readily detectable by using confocal microscopy [3].
• This arrangement of the expression domains of the two genes along the proximal-toward-distal axis of increasing follicular differentiation correlates with the sequential expression of first Hoxc13 and then Hoxc12 [5].
• In Pax9-deficient mice filiform papillae lack the anterior-posterior polarity, a defect that is associated with temporal-spatial changes in Hoxc13 expression [9].

Analytical, diagnostic and therapeutic context of Hoxc13

• Mice carrying mutant alleles of Hoxc13 have been generated by gene targeting [2].
• To identify some of the genetic pathways affected by Hoxc13 overexpression in hair, we performed large-scale differential gene expression analysis on the skin of 5-d GC13 versus normal FVB mice using DNA chip assays [8].

References