E-MTAB-5442 - Ablation of casein kinase 1 in keratinocytes induces p53-dependent hyperpigmentation of the skin
Submitted on 27 February 2014, last updated on 25 August 2017, released on 25 August 2017
To characterize the role of CK1 (encoded by Csnk1a1) in skin physiology, we crossed mice with floxed Csnk1a1 with mice expressing K14CreERT2 to generate mice in which tamoxifen induces the deletion of Csnk1a1 exclusively in keratinocytes (SKO). In addition, we established K14CreERT2 CK1/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 CK1 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.
RNA-seq of coding RNA, compound treatment design, genetic modification design, replicate design
Che-Jung Kuo, Chung-Hsing Chang, Irit Alkalay, Kazumasa Wakamatsu, Marco Mernberger <firstname.lastname@example.org>, Min-Hsi Chiou, Shosuke Ito, Si-Tse Jiang, Takamichi Ito, Thorsten Stiewe, Yinon Ben-Neriah, Yu-Sa Su