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Transcription profiling of mouse skin from epithelial activated beta-catenin mutant embryo

ABSTRACT: Î²-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.

ORGANISM(S): Mus musculus

SUBMITTER: Sarah Millar

PROVIDER: E-GEOD-10726 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of mouse dermis from epithelial activated beta-catenin mutant embryo

Project description:Î²-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

Transcription profiling of mouse epidermis from epithelial activated beta-catenin mutant embryo

Project description:Î²-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

Expression data from skin of epithelial activated beta-catenin mutant mouse embryo

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. Keywords: Genetic modification

2008-05-20 | GSE10726 | GEO

Expression data from epidermis of epithelial activated beta-catenin mutant mouse embryo

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. Keywords: Genetic modification

2008-05-20 | GSE10728 | GEO

Expression data from dermis of epithelial activated beta-catenin mutant mouse embryo

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. Keywords: Genetic modification

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SMARCA4 loss and mutated β-catenin induce proliferative lesions in the murine embryonic cerebellum [scRNA-seq]

Project description:Almost all medulloblastomas (MB) of the Wingless/Int-1 (WNT) type are characterized by hotspot mutations in CTNNB1, and mouse models have convincingly demonstrated the tumor-initiating role of these mutations. Additional alterations in SMARCA4 are detected in around 20% of WNT MB, but their functional role is mostly unknown. We therefore amended previously described Blbp cre::Ctnnb1(ex3)fl/wt mice by the introduction of a floxed Smarca4 allele. Unexpectedly, mutated β-catenin on its own induced severe developmental phenotypes in Blbp cre::Ctnnb1(ex3)fl/wt mice in our hands, including a thinned cerebral cortex, hydrocephalus, missing cerebellar layering, and non-proliferative cell accumulations in the brain stem and cerebellum. An additional loss of SMARCA4 even resulted in prenatal death for most mice. Respective Blbp cre::Ctnnb1(ex3)fl/wt::Smarca4fl/fl mutants developed large proliferative lesions in the cerebellum evolving from E13.5 to E16.5. Histological and molecular analysis of these lesions by DNA methylation profiling and single-cell RNA sequencing suggested an origin in early undifferentiated SOX2-positive cerebellar progenitors. Furthermore, upregulated WNT signaling, altered actin/cytoskeleton organization, and reduced neuronal differentiation were evident in mutant cells. In vitro, cells harboring alterations in both Ctnnb1 and Smarca4 were negatively selected and did not show tumorigenic potential after transplantation in adult recipient mice. However, in cerebellar explant cultures, mutant cells displayed significantly increased proliferation, suggesting an important role of the embryonic microenvironment in the development of lesions. Altogether, these results represent an important first step towards the unravelling of tumorigenic mechanisms induced by aberrant WNT signaling and SMARCA4 deficiency.

2024-04-17 | GSE241018 | GEO

SMARCA4 loss and mutated β-catenin induce proliferative lesions in the murine embryonic cerebellum

Project description:Almost all medulloblastomas (MB) of the Wingless/Int-1 (WNT) subgroup are characterized by hotspot mutations in CTNNB1, and mouse models have convincingly demonstrated the tumor-initiating role of these mutations. Additional alterations in SMARCA4 are detected in around 20 % of WNT MB but their functional role is mostly unknown. We therefore amended previously described Blbp-cre::Ctnnb1(ex3)fl/wt mice by the introduction of a floxed Smarca4 allele. In contrast to existing literature, even mutated β-catenin on its own in our Blbp-cre::Ctnnb1(ex3)fl/wt mice induced severe developmental phenotypes including a thinned cerebral cortex, hydrocephalus, missing cerebellar layering, and non-proliferative cell accumulations in brain stem and cerebellum. An additional homozygous loss of SMARCA4 even resulted in prenatal death for most mice. Interestingly, Blbp-cre::Ctnnb1(ex3)fl/wt::Smarca4fl/fl mutants developed big proliferative lesions in the cerebellum that evolved from E13.5 to E16.5. Histological and molecular analysis of these lesions by DNA methylation analysis and single-cell RNA sequencing suggest an origin in early undifferentiated SOX2-positive cerebellar progenitors. Furthermore, upregulation of WNT signaling and altered actin/cytoskeleton organization and neuronal differentiation were evident in mutant cells. In vitro, cells harboring alterations in both Ctnnb1 and Smarca4 were negatively selected and did not show tumorigenic potential after transplantation in adult recipient mice. However, mutant cells displayed increased proliferation compared to controls in cerebellar explant culture, indicating an important role of the embryonic microenvironment in the development of lesions. Altogether, these results represent an important first step in unravelling tumorigenic mechanisms induced by aberrant WNT signaling and a SMARCA4 deficiency.

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A mouse model for embryonal tumors with multilayered rosettes uncovers the therapeutic potential of Sonic-hedgehog inhibitors

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2017-09-11 | GSE103348 | GEO

Analysis of liver sinusoidal endothelial cells (LSECs) with β-catenin (Ctnnb1) activation

Project description:Endothelial-derived Wnt/Ctnnb1-signaling is an important angiocrine regulator. Ctnnb1 gain-of-function (GOF) in liver sinusoidal endothelial cells was generated by crossing Clec4g-iCre (Wohlfeil SA et al, 2019, Cancer Research) with Ctnnb1(Ex3) fl/fl mice (Harada N et al, 1999, EMBO J) to analyze the effects of endothelial β-catenin signaling on LSEC differentiation and liver function We used microarrays to detail the global programme of gene expression in liver sinusoidal endothelial cells with β-catenin (Ctnnb1) gain-of-function compared to control animals.

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