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Fig. 3. Arnt-null skin phenotype in mice. (A-1) The Arnt^/:Cre⁺ newborn (on the left) is smaller and does not have milk in its stomach in contrast to control littermate (on the right; milk is seen through transparent skin). (A-2) Skin permeability assay (X-gal) in Arnt^flox/flox (Cre^-) and Arnt^/ fetuses (E18.5). In Arnt^/ fetuses, the permeability barrier is impaired with most effect in the throat, chest and groin regions. Control fetus (on the left) has a fully functional barrier and does not show any X-gal penetration. (B) Skin histology (Hematoxylin and Eosin staining) in Arnt^/ (B-1) and control (B-2) newborn mice. Note the thinner epidermis, loss of the granular layer, compact corny layer and prominent parakeratosis in Arnt^/ epidermis. (C) Grafting of Arnt-null skin onto SCID mice. 30 days after grafting, Arnt^/ grafts (C-1) show lower rates of hair growth compared to control grafts (C-2). (C-3) Immunohistochemistry with anti-Arnt antibodies revealed the total absence of Arnt expression in epithelial (K14-positive) compartment of Arnt-null skin including sebaceous gland (arrows) and HF (C-5) whereas the mesenchymal component including dermal fibroblasts, perifollicular dermal sheath and dermal papilla cells of the HF (K14-negative structures) are positive for Arnt. Control skin had normal patterns of Arnt expression in both, epithelial and mesenchymal compartments (C-4,C-6). No difference in HF morphology between Arnt-null and wild-type grafts was observed. Bars, 40 µm.

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