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Genome-wide analysis of epidermal gene expression from Presenilin (1&2)-null, RBPjk-null and wild-type litter mates

ABSTRACT: Analysis of differential gene expression in Psen-null and RBPjk-null epidermal keratinocytes. The hypothesis tested in the present study was that canonical Notch signals could be present at the beginning of epidermal stratification (E13.5) in the RBPj-null epidermis. If an early signal was preserved by epigenetic memory, E18.5 RBPj-null epidermis would resemble the wild-type at the transcriptional level.

ORGANISM(S): Mus musculus

PROVIDER: GSE77813 | GEO | 2016/02/29

SECONDARY ACCESSION(S): PRJNA311608

REPOSITORIES: GEO

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Genome-wide analysis of epidermal gene expression from Presenilin (1&2)-null, RBPjk-null and wild-type litter mates

Project description:Analysis of differential gene expression in Psen-null and RBPjk-null epidermal keratinocytes. The hypothesis tested in the present study was that canonical Notch signals could be present at the beginning of epidermal stratification (E13.5) in the RBPj-null epidermis. If an early signal was preserved by epigenetic memory, E18.5 RBPj-null epidermis would resemble the wild-type at the transcriptional level. Total RNA obtained from 3xRBPj-null and 3xPsen-null epidermis at E18.5 and compared to wild-type (3xRBPjwt & 3xPsenwt) epidermis from littermates.

2016-02-29 | E-GEOD-77813 | biostudies-arrayexpress

Genome-wide analysis of total skin gene expression from presenilin (1&2)-null (PSmut), RBPjk-null (RBPjmut), Presenilin (1&2)-RBPjk-null (PSRmut) and wild-type (WT) littermates

Project description:Analysis of differential gene expression of total skin from different Notch signaling pathway mutants (specifically PSmut, RBPjmut, and PSRmut). Preselin1&2 are the core components of g-secretase enzyme which essential for the Notch receptor activation. RBPjk is the DNA-binding partner of the Notch Intracellular Domain. The hypothesis tested in the present study was RBPjmut skin would resemble the wild-type skin at the transcriptional level, since RBPjmut mice exhibit milder phenotype than PSmut or PSRmut mice.

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Genome-wide analysis of total skin gene expression from presenilin (1&2)-null (PSmut), RBPjk-null (RBPjmut), Presenilin (1&2)-RBPjk-null (PSRmut) and wild-type (WT) littermates

2016-02-29 | E-GEOD-77887 | biostudies-arrayexpress

Comparison of gene expression profiles of p63 null skin versus wild type skin

Project description:In the absence of p63 expression, the epidermis fails to commit to stratification, resulting in aborted skin development. In this study, gene expression profiles of E18.5 p63 null and wt skin, were compared in an effort to identify genes that are directly or indirectly regulated by p63. Keywords: Genetically modified mice

2005-12-10 | GSE3108 | GEO

Transcription profiling of skin from p63 null and wild type mice to identify genes that are directly or indirectly regulated by p63.

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Quantitative Analysis of Notch mutant (Notch1&2-null, Psen1&2-null, RBPjk-null) and wild-type hair follicle transcriptomes by NGS

2016-02-29 | GSE77997 | GEO

Quantitative Analysis of Notch mutant (Notch1&2-null, Psen1&2-null, RBPjk-null) and wild-type hair follicle transcriptomes by NGS

Project description:The goals of this study is to test whether NICD presence protects the RBPjk-null Hair Follicles by altering gene expression via association with other DNA binding proteins at P3, just before the conversion to TSLP-producing keratin cysts. Methods: Skin samples were embedded in OCT. Sectioned at 20Î¼m thickness. Dehydrated in EtOH, and equilibrated to Xylene before the LCM procedure. Laser capture was performed with Arcturus Veritas. Methods: ~100 hair follicles from Notch-null, PS-null, RBPjk-null and wild-type samples were pooled into 3 biological replicates for each genotype and subjected to RNA isolation followed by RNA-Seq. Conclusions: A total of 2047 genes were differentially expressed (â?¥1.5 fold) in three or more biological replicates of Notch mutant hair follicles compared to wild-type controls (p-value<0.05). Unsupervised hierarchical clustering analysis failed to distinguish between the mutants.

2016-02-29 | E-GEOD-77997 | biostudies-arrayexpress

Gene expression profile of E18.5 epidermis from WT and MafB KO mice

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Transcripts identified by microarray analysis that were deregulated in E18.5 Tbx18(cre/+);Rbpj(fl/fl) (Rbpj-cKO) ureters

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Ablation of coactivator Med1 regulates bulge keratinocyte stem cells and accelerates epidermal regeneration after injury [10wk skin]

Project description:Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration. We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=4 WT and KO (each sample contain RNA from one mouse)

2014-01-01 | E-GEOD-50671 | biostudies-arrayexpress

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