Beta-catenin-activated mouse liver primary cancers
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB44400 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5753980_1.fastq.gz | Fastqsanger.gz | |||
| ERR5753980_2.fastq.gz | Fastqsanger.gz | |||
| ERR5753990_1.fastq.gz | Fastqsanger.gz | |||
| ERR5753990_2.fastq.gz | Fastqsanger.gz | |||
| ERR5754000_1.fastq.gz | Fastqsanger.gz |
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Project description:β-catenin signaling can be both a physiological and an oncogenic pathway in the liver. It controls compartmentalized gene expression, allowing the liver to ensure its essential metabolic function. It is activated by mutations in 20 to 40% of hepatocellular carcinomas with specific metabolic features. We decipher the molecular determinants of β-catenin-dependent zonal transcription using mice with β-catenin-activated or -inactivated hepatocytes, characterizing in vivo their chromatin occupancy by Tcf4 and β-catenin, their transcriptome and their metabolome. We find that Tcf4 DNA-bindings depend on β-catenin. Tcf4/β-catenin binds Wnt-responsive elements preferentially around β-catenin-induced genes. In contrast, genes repressed by β-catenin bind Tcf4 on Hnf4-responsive elements. β-catenin, Tcf4 and Hnf4α interact, dictating β-catenin transcription which is antagonistic to that elicited by Hnf4α. Finally, we find the drug/bile metabolism pathway to be the one most heavily targeted by β-catenin, partly through xenobiotic nuclear receptors. We conclude that β-catenin patterns the zonal liver together with Tcf4, Hnf4α and xenobiotic nuclear receptors. This network represses lipid metabolism, and exacerbates glutamine, drug and bile metabolism, mirroring hepatocellular carcinomas with β-catenin mutational activation. In vivo liver samples in 4 conditions: Betacat activated (WCE, Tcf4 chipseq, Betacat chipseq, mRNAseq with 2 replicates), Betacat null (WCE, Tcf4 chipseq, mRNAseq with 2 replicates), Betacat control (mRNAseq with 2 replicates), Wild type (mRNAseq with 2 replicates)
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Project description:We generated a murine genetic model of beta-catenin deficiency targeted to the ureteric bud cell lineage to study the role of beta-catenin mediated Wnt signaling during ureteric morphogenesis. Experiment Overall Design: A comparison was made between triplicate samples of E12.5 kidneys from either normal mice or mice with a b-catenin allele containing LoxP sites flanking exons 2 through 6 crossed to Hoxb7-Cre:Gfp mice
2008-04-04 | E-GEOD-9629 | 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 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.
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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 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.
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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 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.
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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 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
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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. Keywords: Genetic modification
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Project description:Oncogenic stabilizing mutations in the beta-catenin gene CTNNB1 are common in one class of human Wilms tumors. To model these tumors, we crossed mice carrying an inducible Cre recombinase (Rosa26-CreERT2) with a conditional gain-of-function beta-catenin allele (Ctnnb1Ex3flox). We obtained kidneys at embryonic day 13.5 and placed them in organ culture with tamoxifen. Multiple small tumors formed in the Ctnnb1∆Ex3 kidneys while the control kidneys developed normally. Immunostaining for Sall1, a marker of condensing metanephric mesenchyme, indicated that the tumors arise from this tissue compartment, analogous to the origin of human Wilms tumors. Expression profiling identified a set of induced genes overlapping with those up-regulated in human Wilms tumors with CTNNB1 mutations, including genes encoding feedback inhibitors of Wnt/beta-catenin signaling, the epithelial-mesenchymal transition (EMT) inducers, and the transcription factor E2-2 (ITF2/TCF4). A conditional deletion of E2-2 showed that this gene is important for growth of the nephroblastomas, in part via promoting an epithelial to mesenchymal transition downstream of beta-catenin. Given these cross-species validations, and genetic proof of the oncogenic function of a key downstream target gene, we expect that this rapid and efficient organ culture model will be useful for further studies to dissect and inhibit oncogenic Wnt/beta-catenin signaling.
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