Transcription profiling of mouse skin, dermis, and epidermis of epithelial activated beta-catenin mutant embryo
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Sarah Millar
PROVIDER: E-GEOD-10733 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:β-catenin signaling is required for hair follicle development, but it is unknown whether it is sufficient to activate expression of hair follicle genes in embryonic skin. To address this we profiled gene expression in dermis from E15.5 KRT14-Cre Ctnnb1(Ex3)fl/+ embryos carrying an activating mutation in epithelial beta-catenin, and control littermate embryos. Experiment Overall Design: Total dermal RNA from two KRT14-Cre Ctnnb1(Ex3)fl/+ and two control littermate E15.5 embryos was hybridized to Affymetrix GeneChip Mouse Genome MOE430 2.0 oligonucleotide microarrays. Experiment Overall Design: Appended below is Table S2: Full list of differentially expressed genes in KRT14-Cre Ctnnb1(Ex3)fl/+ mutant compared with control littermate dermis at E15.5, including normalization and filter parameters. Fold change, listed in the second column, gives the ratio of normalized mutant : control transcript levels.
2008-06-20 | E-GEOD-10727 | biostudies-arrayexpress
Project description:β-catenin signaling is required for hair follicle development, but it is unknown whether it is sufficient to activate expression of hair follicle genes in embryonic skin. To address this we profiled gene expression in epidermis from E15.5 KRT14-Cre Ctnnb1(Ex3)fl/+ embryos carrying an activating mutation in epithelial beta-catenin, and control littermate embryos. Experiment Overall Design: Total epidermal RNA from two KRT14-Cre Ctnnb1(Ex3)fl/+ and two control littermate E15.5 embryos was hybridized to Affymetrix GeneChip Mouse Genome MOE430 2.0 oligonucleotide microarrays. Experiment Overall Design: Appended below is Table S1: Full list of differentially expressed genes in KRT14-Cre Ctnnb1(Ex3)fl/+ mutant compared with control littermate epidermis at E15.5, including normalization and filter parameters. Fold change, listed in the second column, gives the ratio of normalized control : mutant transcript levels.
2008-06-20 | E-GEOD-10728 | biostudies-arrayexpress
Project description:β-catenin signaling is required for hair follicle development, but it is unknown whether it is sufficient to activate expression of hair follicle genes in embryonic skin. To address this we profiled gene expression in skin dissected from E14.5 KRT14-Cre Ctnnb1(Ex3)fl/+ embryos carrying an activating mutation in epithelial beta-catenin, and control littermate embryos. Experiment Overall Design: Total skin RNA from two KRT14-Cre Ctnnb1(Ex3)fl/+ and two control littermate E14.5 embryos was hybridized to Affymetrix GeneChip Mouse Genome MOE430 2.0 oligonucleotide microarrays. Experiment Overall Design: Appended below is Table S3: Full list of differentially expressed genes in KRT14-Cre Ctnnb1(Ex3)fl/+ mutant compared with control littermate intact skin at E14.5, including normalization and filter parameters. Fold change, listed in the second column, gives the ratio of normalized mutant : control transcript levels.
2008-06-20 | E-GEOD-10726 | biostudies-arrayexpress
Project description:The vitamin D receptor (VDR) regulates cell proliferation and differentiation including epidermal keratinocytes by modulating transcription of its target genes. We are investigating the role of VDR in epidermal stem cells and their progenies in the regeneration process of epidermis and hair in the skin. VDR null mice are utilized in which VDR is specifically deleted in keratin 14 (K14) expressing keratinocytes by Cre-lox strategy. The impact of VDR deletion was evaluated by comparison of VDR null mice with no cre littermate control mice. The VDR was abundantly expressed in potential epidermal stem cells including basal cells in interfollicular epidermis (IFE), and in CD34 expressing bulge keratinocytes in hair follicles. Gene expression profiles and subsequent pathway analysis of stem cell enriched keratinocyte populations revealed that the VDR deletion significantly suppressed β-catenin signaling as well as VDR signaling. The role of VDR in epidermal stem cells was studied during hair follicle cycling and wound healing processes. The epidermal stem cells were not appropriately stimulated by hair depilation, and did not reinitiate anagen in the hair follicles resulting in a failure of hair regrowth. In addition, the stem cells were not fully activated after full thickness wounds were generated in VDR null skin under a low calcium diet to suppress compensation pathways. Cell proliferation was not fully induced in potential stem cells located in both IFE and hair follicles near the wounding edges, and re-epithelialization rate was delayed in VDR null skin. Gene expression profiling of the wounded skin (3 days after injury) indicated that β-catenin signaling was not fully induced in VDR null skin comparable to that observed in β-catenin null mice. The β-catenin target genes including Axin2 and cell cycle regulators involved in epidermal stem cell function were not induced in the edges of the wound of VDR null skin. These results demonstrated that VDR plays an essential role in hair cycling and wound healing processes through regulation of β-catenin signaling in epidermal stem cells and their progenies. n=3 CON and KO (each sample contain RNA extracted from keratinocytes, which is isolated from VDR KO and littermate control skins excised from 3 mice)
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Project description:RABGEF1, a guanine nucleotide exchange factor for Rab5 GTPase, can negatively regulate mast cell activation in vitro. In addition, RabGEF1-deficient mice develop morbidity and severe skin inflammation associated with marked increases in skin mast cell numbers (Tam et al., Nat Immunol, 5(8):844-52, 2004). These findings suggest that over-reactive skin mast cells may contribute to the observed skin pathology in vivo. In order to identify the cell type(s) which contribute to skin inflammation when RabGEF1 is absent, we attempted to delete Rabgef1 gene specifically in three major skin cell types, namely mast cells, myeloid cells and keratinocytes; thus, Rabgef1 floxed (fl/fl) mice were crossed with mice expressing the Cre-recombinase under the influence of the promoter of Mcpt5, LysZ or K14, respectively. Unexpectedly, Mcpt5-Cre;Rabgef1fl/fl and Lysz-Cre;Rabgef1fl/fl mice appeared normal without phenotypic abnormalities. However, K14-Cre;Rabgef1fl/fl mice were normal at birth but rapidly developed morbidity and skin inflammation after 2-3 days, and died between 1 and 8 weeks of age. Skin (epidermis + dermis) was sampled from the center of the back behind shoulders, for 2 conditional knock-out mice (Rabgef1 lox/lox K14-Cre, hereafter called Rabgef1K-KO) and 2 control mice (Rabgef1 lox/lox). Total RNA was isolated from mouse skin using Trizol. Gene expression analysis was performed using Affymetrix Mouse Genome 430 2.0 arrays, with two replicates per genotype. Microarray data were analysed using Bioconductor for R.
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