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RNA-sequencing of FACS-sorted Prominin1+ radial glial cells of E12.5 SmadNes mutant embryos (Smad1wt/fl;Smad5wt/fl;Nestin:Cre+/0) and control littermates (Smad1wt/fl;Smad5wt/fl;Nestin:Cre0/0)

ABSTRACT: We report the transcriptomes of mouse E12.5 cortical radial glial cells and the changes caused by inhibition of the canonical BMP signalling effectors SMAD1/5, whose expression levels are reduced by 50% in the SmadNes mutants.

ORGANISM(S): Mus musculus

PROVIDER: GSE153751 | GEO | 2020/07/04

REPOSITORIES: GEO

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RNA-sequencing of FACS-sorted Prominin1+ radial glial cells of E12.5 SmadNes mutant embryos (Smad1wt/fl Smad5wt/fl Nestin:Cre+/0) and control littermates (Smad1wt/fl Smad5wt/fl Nestin:Cre0/0)

Project description:RNA-sequencing of FACS-sorted Prominin1+ radial glial cells of E12.5 SmadNes mutant embryos (Smad1wt/fl Smad5wt/fl Nestin:Cre+/0) and control littermates (Smad1wt/fl Smad5wt/fl Nestin:Cre0/0)

| PRJNA643971 | ENA

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

Project description:We use mice containing a gene trap in the first intron of the Rest gene, which effectively eliminates transcription from all coding exons, to prematurely remove REST from neural progenitors. We find catastrophic DNA damage that occurs during S-phase of the cell cycle, with consequences including abnormal chromosome separation, apoptosis, and smaller brains. Further support for persistent effects is the latent appearance of proneural glioblastomas in adult mice also lacking the tumor suppressor, p53. A Rest deficient mouse line generated previously, using a conventional gene targeting approach, does not exhibit these phenotypes, likely due to a remaining C terminal peptide that still binds chromatin and recruits REST chromatin modifiers.Our results indicate that REST-mediated chromatin remodeling is required for proper S-phase dynamics, prior to its well-established role in relieving repression of neuronal genes at terminal differentiation. extract RNA from E12.5 brain in triplicates, compare gene expression profile between Gene Trap REST knockout mice and control littermates

2015-08-01 | E-GEOD-68368 | biostudies-arrayexpress

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

2015-08-01 | GSE68368 | GEO

Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl in heart at E11.5 and E12.5

Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from a Mesp1Cre driven ablation of Hira in the heart at E11.5 and E12.5. Methods: RNA extraction was done in triplicate from Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl embryonic hearts at E11.5 and E12.5 using the QIAGEN RNeasy mini kit. RNAseq was processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R package. Strand NGS 2.5 software was used to re-analyse the aligned files (.bam). By applying the Mann Whitney unpaired test, Benjamini Hochberg False discovery rate (FDR) and filtering the genes using adjusted p-value ≤ 0.05 and absolute fold change ≥ 1.5, 95 % of the results were identical to the DEseq package used by the UCL Genomics facility. Results: We identified 360 coding transcripts changed in the mutant hearts (Mann Whitney unpaired test, Benjamini Hochberg FDR, p ≤ 0.05, FC ≥ 1.5) with no trend towards up- or down-regulation of global transcription (48.8% down vs 51.2% up) at E12.5. Conclusions: This work analyses the role of HIRA in mouse cardiac development. It was found that Tnni2 is the most upregulated gene in the absence of Hira. qRT-PCR validation of 25 targets. Little (<5%) or no variation of fold change between RNAseq and qRT-PCR data were observed.

2016-08-12 | GSE79937 | GEO

AP-2α pull down from E12.5 cortex

Project description:Identificatin of interaction partners of AP-2α via pull down from the cortex of E12.5 mice followed by quantitative mass spectrometry.

2023-12-11 | PXD047202 | Pride

Effect of c-Maf mutation on Mafb-GFP-positive FACS-purified cells in the E12.5 mouse gonad

Project description:Morphogenesis of the gonad requires cell-cell adhesion changes between diverse cell types. In the Drosophila gonad, the gene traffic jam regulates cell adhesion changes required for gonad formation and germ cell development (Li et al., 2003. Nature Cell Biol). To determine if the mammalian homologs of traffic jam in mammals, c-Maf and Mafb, also play a role in the transcription regulation of cell adhesion molecules in the mouse gonad, we performed a microarray analysis of FACS-purified Mafb-GFP-positive cells in E12.5 male control and c-Maf/Mafb mutant gonads. We used microarrays to determine genes affected by c-Maf mutation in E12.5 mouse gonad/mesonephros interstitial cells and macrophages

2013-11-20 | GSE41715 | GEO

RNAseq Analysis of Transcriptome expression profiles in E12.5 and E13.5 FACS sorted Osr2RFP/- (mutant)and Osr2RFP/+ (control) palatal mesenchymal cells

Project description:Purpose: The purpose of this study is to compare the transcriptome expression profiles of E12.5 and E13.5 Osr2RFP/- and Osr2RFP/+ palatal mesenchyme by using RNA-seq analysis. Methods: Osr2RFP/+ male mice were crossed with Osr2+/- female mice. The embryos were harvested at E12.5 and E13.5. The pair of palatal shelves were dissected from each Osr2-RFP positive embryo. The RFP+ palatal mesenchyme cells were isolated by using fluorescence-activated cell sorting (FACS). RNA-seq analysis was carried out using the FACS-isolated palatal mesenchyme from Osr2RFP/- and Osr2RFP/+ embryos, respectively.

2018-02-13 | GSE95638 | GEO

Effect of c-Maf mutation on Mafb-GFP-positive FACS-purified cells in the E12.5 mouse gonad

2013-11-20 | E-GEOD-41715 | biostudies-arrayexpress

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi vs Rest GTi/GTi litermates

2015-08-01 | E-GEOD-68459 | biostudies-arrayexpress

E12.5 Neural tube RNA-Seq

Project description:E12.5 Neural tube RNA-Seq

| PRJNA547355 | ENA