Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNA-seq study of Eed-deleted cerebellar granule neuron progenitors (CGNPs)

ABSTRACT: We studied CGNPs with conditional deletion of Eed using scRNA-seq. Eed was deleted in CGNPs by crossing Math1-Cre mice with Eed floxed mice. scRNA-seq seq was performed by Drop-seq. The results may be compared to our prior published data on scRNA-seq in normal CGNPs (GEO accession number GSE129730)

ORGANISM(S): Mus musculus

PROVIDER: GSE207451 | GEO | 2022/07/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

scRNA-seq study of Eed-deleted cerebellar granule neuron progenitors (CGNPs)

Project description:scRNA-seq study of Eed-deleted cerebellar granule neuron progenitors (CGNPs)

| PRJNA855640 | ENA

Genome-wide gene expression profile of mouse proliferating / differentiating cerebellar granular progenitor cells (CGNPs)

Project description:To study the gene expression changes during neuronal differentiation of mouse cerebellar granular progenitor cells (CGNPs), we generated neurospheres (proliferating CGNPs) and differentiated the cells (differentiating CGNPs). Then we performed RNA-Seq analysis.

2022-05-04 | GSE196548 | GEO

Atr maintains chromosomal integrity during postnatal cerebellar neurogenesis [Affymetrix]

Project description:Microcephaly and medulloblastoma result from mutations that compromise genomic stability. We report that Atr, which is mutated in the microcephalic disorder Seckel syndrome, is required to maintain chromosomal integrity during postnatal cerebellar neurogenesis. Atr deletion in cerebellar granule neuron progenitors (CGNPs) induced proliferation-associated DNA damage, p53 activation, apoptosis, and cerebellar hypoplasia. Co-deletions of either Bax and Bak or p53 prevented apoptosis in Atr-deleted CGNPs, but failed to fully rescue cerebellar growth. Atr-deficient CGNPs showed impaired cell cycle checkpoint function and continued to proliferate, accumulating chromosomal abnormalities. RNA-Seq demonstrated that the transcriptional response to Atr-deficient proliferation was p53-driven. Acute Atr inhibition in vivo by nanoparticle-formulated VE-822 reproduced the disruptions seen with Atr deletion. Our data show that p53-driven apoptosis and senescence, and non-apoptotic cell death redundantly limit growth in Atr-deficient progenitors. These overlapping mechanisms that suppress growth in Atr-disrupted CGNPs may be exploited for treatment of CGNP-derived medulloblastoma using Atr inhibition.

2016-09-01 | GSE85393 | GEO

Atr maintains chromosomal integrity during postnatal cerebellar neurogenesis [RNA-Seq]

2016-09-01 | GSE83720 | GEO

The Central Role of EED in the Orchestration of Polycomb Group Complexes

Project description:Polycomb Repressive Complexes 1 and 2 (PRC1 and 2) play a critical role in the epigenetic regulation of transcription during cellular differentiation, stem cell pluripotency, and neoplastic progression1-3. Here we show that the Polycomb group protein EED, a core component of PRC2, physically interacts with and functions as part of the PRC1 complex. Components of PRC1 and PRC2 compete for EED binding. EED functions to recruit PRC1 to H3K27me3 loci and enhances PRC1 mediated H2A ubiquitin E3 ligase activity. Taken together, we uncover the integral role of EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2. EED, uH2A, RING1A, RING1B, BMI1 and H3K27Me3 ChIP-seq in EED stable knockdown and control Scramble DU145 prostate cancer cell line

2014-01-23 | E-GEOD-42566 | biostudies-arrayexpress

Bulk RNA-seq of Colonic Epithelia from EED and EED/Satb2 Double Knockout Mice

Project description:Bulk RNA-seq of Colonic Epithelia from EED and EED/Satb2 Double Knockout Mice

| PRJNA746272 | ENA

Transcriptional repression by non-canonical EED stimulation of histone deacetylase activity is required for heart maturation independently of H3K27me3 [RNA-seq for EED and HDAC rescue]

Project description:Through H3K27me3 and H3K27ac ChIP-seq and RNA-seq data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.

2017-04-14 | GSE89585 | GEO

Polycomb protein EED is required for selective silencing of pluripotency genes upon ESC differentiation

Project description:Eed (embryonic ectoderm development) is a core component of the Polycomb Repressive Complex 2 (PRC2) which catalyzes the methylation of histone H3 lysine 27 (H3K27). Trimethylated H3K27 (H3K27me3) can act as a signal for PRC1 recruitment in the process of gene silencing and chromatin condensation. Previous studies with Eed KO ESCs revealed a failure to down-regulate a limited list of pluripotency factors in differentiating ESCs. Our aim was to analyze the consequences of Eed KO for ESC differentiation. To this end we first analyzed ESC differentiation in the absence of Eed and employed in silico data to assess pluripotency gene expression and H3K27me3 patterns. We linked these data to expression analyses of wildtype and Eed KO ESCs. We observed that in wildtype ESCs a subset of pluripotency genes including Oct4, Nanog, Sox2 and Oct4 target genes progressively gain H3K27me3 during differentiation. These genes remain expressed in differentiating Eed KO ESCs. This suggests that the deregulation of a limited set of pluripotency factors impedes ESC differentiation. Global analyses of H3K27me3 and Oct4 ChIP-seq data indicate that in ESCs the binding of Oct4 to promoter regions is not a general predictor for PRC2-mediated silencing during differentiation. However, motif analyses suggest a binding of Oct4 together with Sox2 and Nanog at promoters of genes that are PRC2-dependently silenced during differentiation. In summary, our data further characterize Eed function in ESCs by showing that Eed/PRC2 is essential for the onset of ESC differentiation. RNAs obtained from undifferentiated (d0) wild type and Eed KO ESCs and from day 3 (d3) and day 7 (d7) respective Ebs were subjected to Affymetrix Mouse Gene 1.0 ST Array. 24 samples in total.

2014-08-28 | E-GEOD-49305 | biostudies-arrayexpress

Next-generation sequencing Facilitates Quantitative Analysis of Wild Type and EED-/- mice cerebellum Transcriptomes and Genome-wide maps of chromatin state in Wild Type and EED-/- mice cerebellum

Project description:Purpose: The goals of this study are to compare Wild Type and EED-/- cerebellum transcriptome profiling (RNA-seq) to quantitative reverse transcription polymerase chain reaction (qRT–PCR) differentially expressed genes and find target genes. We performed chromatin-immunoprecipitation coupled to sequencing (ChIP-seq) to dissect the relationship between the differentially expressed genes and the occupancy of H3K27me3, H3K27ac and EED. Methods: Cerebellum mRNA profiles of 14-day-old(P14) wild-type (WT) and Embryonic Ectoderm Development conditional knockout (EED-/-) mice were generated by deep sequencing, in triplicate,using Illumina HiSeq 2500 system.All RNA-Seq data were aligned to mouse genome version mm10 using Salmon (v.1.1.0) .We use cluster software and Euclidean distance matrix for the hierarchical clustering analysis of the expressed gene and sample program at the same time, the clustering results can be viewed with javaTreeview. qRT–PCR validation was performed using SYBR Green assays. we performed ChIP-seq using freshly isolated P14 from Wild Type and EED-/- cerebellar tissues . DNA libraries generated from ChIP-DNA and input-DNA were deep-sequenced using HiSeq single-end 50bp. Results:Only transcripts that showed more than 1.5-fold differential expression compared to control were subjected to relevance network analysis. 3149 candidate genes that were differentially expressed with biological functional groups as compared between WT and EED-/- mice .We found that the enrichment of H3K27me3 was decreased H3K27ac was highly increased in EED-/- mice. Conclusions: Our study represents the first detailed analysis of Wild Type and EED-/ mice cerebellum transcriptomes, with three biologic replicates, generated by RNA-seq technology. We report the application of ChIP-sequencing technology for high-throughput profiling of histone modifications in cerebellar cells.

2024-04-02 | GSE169312 | GEO

ChIP-Seq Analysis of Eed hypo/wt

Project description:ChIP-Seq Analysis of Eed hypo/wt

| PRJEB12273 | ENA