The tissue specific ablation of the Notchl receptor in mouse epidermis leads to hyperplasia in the epidermis, the development of tumors and an increased susceptibility to chemical carcinogens – thus indicating that Notch acts as a tumor suppressor in mammal skin [ 40].
Deletion of one Hdac1 allele in Hdac2Δ/Δep epidermis or one Hdac2 allele in Hdac1Δ/Δep epidermis led to the corresponding reduction in mRNA levels (Supplementary Figure S2B).
Embryonic deletion of both Jun and JunB within the epidermis leads to fatal cachexia of neonatal mice (Guinea-Viniegra et al, 2009; Zenz et al, 2005).
For example, IKKβ ablation in the skin epidermis leads to auto-immune diseases of the skin, precluding the use of the knockout mice to study wound healing [7], whereas, IKKβ ablation in intestinal epithelium results in aberrant epithelial cell survival and proliferation in a number of injury models [15], [40].
In the mouse epidermis, a similar complex of spindle orientation proteins localizes at the apical cortex to drive the asymmetric divisions that lead to the stratification and differentiation of the skin (Lechler and Fuchs, 2005; Poulson and Lechler, 2010).
TC45 was also primarily localized in the cytoplasm of mouse epidermis (data not shown).
Since low H4 acetylation was common in stem cells in human interfollicular epidermis (Fig. 1), we examined whether this was also the case in mouse epidermis (Fig. 3A D).
After this, the two lists of differentially expressed genes were crossed, thereby selecting genes that were either down- or up-regulated both in GATA3−/− epidermis (when compared to WT mouse epidermis), as wells as in lesional psoriatic epidermis (when compared to non-lesional epidermis).
SKH-1 mouse epidermis samples were removed from liquid nitrogen snap frozen dorsal skin by scraping on dry ice.
Twenty-five to fifty µg of total protein from mouse epidermis or keratinocytes (control and UVB treated) were resolved using SDS-PAGE.
