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. 2011 May 15;124(10):1681–1690. doi: 10.1242/jcs.077552

Fig. 6.

Fig. 6.

Epidermal-specific Pbx1-null mice are viable and have abnormalities in external but not internal barrier and stratum corneum. (A) Mice generated by keratin-14 Cre-driven epidermal deletion of floxed Pbx1 alleles (Murphy et al., 2010) are healthy and viable until about 4 months of age when they lose hair in stressed regions, for example, around the whisker pad. (B) Western analysis of protein from epidermis or skin (epidermis and dermis) of parental floxed Pbx1 mice (Pbx1f/f) and K14Cre-mediated epidermal Pbx1 deleted mice (K14Cre;Pbx1f/f) shows clear epidermal-specific knockdown of PBX1 protein. (C) Real-time PCR analysis of parental Pbx1f/f and K14Cre;Pbx1f/f epidermal and skin RNA from pups (day 16 to day 22) and adult (3–4 months) mice shows maintenance of epidermal-specific reduction in Pbx1 mRNA, whereas Pbx2 mRNA is slightly, but consistently upregulated. (D) Barrier assay shows lesions on the epidermis of K14Cre:Pbx1f/− mice (arrows), but not on wild-type (not shown) or control K14Cre:Pbx1f/+ mice. K14Cre:Pbx1f/− epidermal stratum corneum is thicker and noncompact (bracket) compared with control stratum corneum. (E) Pbx1-null (K14Cre:Pbx1f/−) tongue epidermis lacks lesions; ventral tongue surface is shown because it lacks blue-staining papillae except at the tip, clearly seen on the tip of control tongue. Tongue stratum corneum of Pbx1-null (K14Cre:Pbx1f/−) does not differ from control. Ep, epidermal; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. Scale bars: 70 μm (D); 100 μm (E).