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Analysis of EMCN+ bone marrow cells in Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice

ABSTRACT: Analysis of EMCN+ bone marrow cells in Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice

PROVIDER: PRJNA748387 | ENA |

REPOSITORIES: ENA

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Analysis of EMCN+ bone marrow cells in Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice

Project description:Endothelial-derived Wnt/Ctnnb1-signaling is an important angiocrine regulator. Ctnnb1 gain-of-function (GOF) in sinusoidal endothelial cells was generated via Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice to analyze the effects of endothelial β-catenin signaling on bone marrow function. We used microarrays to detail the global programme of gene expression in bone marrow EMCN+ cells with β-catenin (Ctnnb1) gain-of-function compared to Wildtype.

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Analysis of terminal erythroid progenitor populations PIII and PIV in Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice

Project description:Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt become anemic by the age of three months. We utilzed this model to investigated effects of niche Wnt-Signaling alterations on the terminal erythroid progenitor populations PIII (polychromatic erythroblasts) and PIV (orthochromatic erythroblasts and reticulocytes) by microarray transcriptome analysis.

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

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m6A-seq analysis of Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) bone-marrow-derived macrophages (BMDMs) transcriptomes after co-culturing with MC38 cells

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Quantitative Analysis of Wild Type,Ctnnb1 deltaEx3 and Ctnnb1 deltaEx2-6 Spinal Cord Transcriptomes

Project description:The goals of this study are to analyze NGS-derived spinal cord transcriptome profiling (RNA-seq) of wild type (WT), Nestin-Cre mediated Ctnnb1 Ex3 deletion (gain of function, dE3) and Ex2-6 deletion (loss of function, cKO) at embryonic day 13.5 (E13.5). Spinal cord RNA profiles were generated by deep sequencing, using Illumina Hiseq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with HISAT2 and RSeQC.

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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

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

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