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Kruppel-like factor 2 is important for endoderm-related gene regulation with Ring1b-mediated mechanism in mESCs

ABSTRACT: Kruppel-like factor 2 is important for endoderm-related gene regulation with Ring1b-mediated mechanism in mESCs

PROVIDER: PRJNA698396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13593635_1.fastq.gz	Fastqsanger.gz
	SRR13593635_2.fastq.gz	Fastqsanger.gz
	SRR13593636_1.fastq.gz	Fastqsanger.gz
	SRR13593636_2.fastq.gz	Fastqsanger.gz
	SRR13593637_1.fastq.gz	Fastqsanger.gz

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Kruppel-like factor 2 is important for endoderm-related gene regulation with Ring1b-mediated mechanism in mESCs

Project description:We report the RNA-seq data of Klf2 KO and Ring1b KD from mouse embryonic stem cells. Wild type and Klf2 knockout cells were knockdowned with Ring1b shRNA. Samples were lysed with total RNA prep kit.

2021-02-01 | GSE165873 | GEO

Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

Project description:This experiment was designed to determine the extent of gene misregulation in mESCs containing catalytically dead Ring1B in comparison to mESCs lacking Ring1B. Polyadenylated mRNA was prepared from wildtype mESCs (WT), mESCs deficient for Ring1B (KO) and mESCs cells containing catalytically dead Ring1B (I53A). Each sample is represented by 3 biological replicate hybridisations.

2015-09-20 | E-GEOD-69824 | biostudies-arrayexpress

Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

Project description:This experiment was designed to determine the extent of gene misregulation in mESCs containing catalytically dead Ring1B in comparison to mESCs lacking Ring1B.

2015-09-20 | GSE69824 | GEO

Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

2015-09-20 | GSE69955 | GEO

Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.

2015-09-20 | E-GEOD-69955 | biostudies-arrayexpress

Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]

Project description:SETD2/HYPB has been known as a histone H3K36 specific methyltransferase. However, its roles in physiology such as development and cellular function remain unclear. In this study, using mESCs as cellular model, we show that Setd2 mainly regulates differentiation of murine embryonic stem cells (mESCs) towards primitive endoderm. This study aimed at exploring how did Setd2 regulate primitive endoderm. differentiation. We used microarrays to detail the global programme of gene expression controled by setd2, which is required for endoderm differentiation. Wild type and Setd2 knockout mESCs were selected for RNA extraction and hybridization on Affymetrix GeneChip® mouse genome 430 2.0 arrays. We sought to obtain some deregulated genes, which were required for primitive endoderm differentiation. For comparison, three biological repeats of each were performed.

2014-10-14 | E-GEOD-54931 | biostudies-arrayexpress

Primitive endoderm differentiation in wild-type and Med12-mutant mESCs [scRNA-seq]

Project description:Cell differentiation results from coordinated changes in gene transcription in response to combinations of signals. FGF, Wnt, and mTOR signals regulate the differentiation of pluripotent mammalian cells towards embryonic and extraembryonic lineages, but how these signals cooperate with general transcriptional regulators is not fully resolved. Here, we report a genome-wide CRISPR screen that reveals both signaling components and general transcriptional regulators for differentiation-associated gene expression in mESCs. Focusing on the Mediator subunit Med12 as one of the strongest hits in the screen, we show that it regulates gene expression in parallel to FGF and mTOR signals. Loss of Med12 is compatible with differentiation along both the embryonic epiblast and the extraembryonic primitive endoderm lineage, but pluripotency transitions are slowed down, and the transcriptional separation between epiblast and primitive endoderm identities is enhanced in Med12-mutant cells. These cellular phenotypes correlate with reduced biological noise upon loss of Med12. These findings suggest that Med12 regulates cellular plasticity through the priming of transcriptional changes during differentiation, thereby modulating the effects of a broad range of signals.

2024-01-25 | GSE253608 | GEO

Primitive endoderm differentiation in wild-type and Med12-mutant mESCs [scRNA-seq]

Project description:Primitive endoderm differentiation in wild-type and Med12-mutant mESCs [scRNA-seq]

| PRJNA1066345 | ENA

Quantitative Analysis of Wild Type(wt) and Setd2 knockout(ko) mESCs Transcriptomes [RNA-Seq]

Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation. One wt and one ko mESCs were generated by deep sequencing, using Illumina GAIIx.

2014-10-14 | E-GEOD-54932 | biostudies-arrayexpress

Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]

2014-10-14 | GSE54931 | GEO