Fig. 8.

Graphical summary describing JunB function in skin. Schematic drawing depicts wild type epidermal cells and their progenitors expressing K14 (left panel, green) and the JunB cKO epidermal cells and their progenitors (right panel, light yellow) in their different epidermal skin compartments (IFE, interfollicular epidermis; SG, sebaceous gland). In the JunB wild type conditions—via Notch signaling—epidermal differentiation and proliferation of cells are balanced even upon different stimuli. This in conjunction with the restriction of epidermal progenitor toward epidermal differentiation guarantees a functional epidermal barrier. By contrast, in the JunB cKO situation, epidermal cells and their progenitors—due to overactivation of Notch signaling—cannot undergo proper differentiation but instead are caught in unrestrained proliferation. Most importantly, JunB cKO epidermal progenitors are not lineage restricted and tweak into the sebocyte differentiation and under conditions of skin irritation/trauma result in de novo sebaceous gland formation. The lineage deviation of epidermal progenitors towards as sebocyte phenotype is accompanied with a functional change and in consequence an increase in the synthesis of mucin at the expense of lipids. In fact, the major enzyme catalyzing wax ester synthesis is decreased. This together with the lack of epidermal differentiation and a change in the outermost composition of the wax impairs the protective barrier of the epidermis. Impairment of JunB function at several molecular and cellular levels results in complex phenotypes like seborrheic like dermatitis, delayed wound healing and loss of skin homeostasis