Ablation of casein kinase 1a in keratinocytes induces p53-dependent hyperpigmentation of the skin

To characterize the role of CK1a (encoded by Csnk1a1) in skin physiology, we crossed mice with floxed Csnk1a1 with mice expressing K14–Cre–ERT2 to generate mice in which tamoxifen induces the deletion of Csnk1a1 exclusively in keratinocytes (SKO). In addition, we established K14–Cre–ERT2 CK1a/p53 double-knockout (DKO) to analyze the effect of coablation of both genes. 4-hydroxy-Tamoxifen was applied for 14 days to induce the deletion of CK1a and/or p53 in the epidermis of the mice. In addition, wild type mice where exposed to UVB irradiation to compare the effect of CK1a ablation with the effects of normal UV exposure. In comparison, we analyzed also wild type mice as reference. RNA was obtained from cells derived from mouse ear dorsal-epidermis and tail skin. Subsequently, we performed RNA sequencing and transcriptome analysis.