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A Co-repressor CBFA2T2 regulates pluripotency and germline development [RNA-seq]

ABSTRACT: In this experiment, we sought to determine how PRDM14 and CBFA2T2 regulate the transcriptome of mouse embryonic stem cells

ORGANISM(S): Mus musculus

PROVIDER: GSE71674 | GEO | 2016/06/03

SECONDARY ACCESSION(S): PRJNA291780

REPOSITORIES: GEO

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A Co-repressor CBFA2T2 regulates pluripotency and germline development [ChIP-seq]

Project description:In this experiment, we sought to determine the relative distribution of CBFA2T2, PRDM14, RING1B POU5F1 and SUZ12

2016-06-03 | GSE71675 | GEO

Co-repressor CBFA2T2 regulates pluripotency and germline development.

Project description: Not available

| S-EPMC4911307 | biostudies-literature

A Co-repressor CBFA2T2 regulates pluripotency and germline development

Project description:A Co-repressor CBFA2T2 regulates pluripotency and germline development

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A Co-repressor CBFA2T2 regulates pluripotency and germline development [ChIP-seq]

Project description:A Co-repressor CBFA2T2 regulates pluripotency and germline development [ChIP-seq]

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A Co-repressor CBFA2T2 regulates pluripotency and germline development

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-06-02 | GSE71676 | GEO

Identification of genes regulated by knockdown of HSF1 or CBFA2T2

Project description:To examine whether the HSF1–CBFA2T2 complex regulates gene expression in human melanoma MeWo cells, DNA microarray analysis was performed.

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A novel histone H3K27 reader, CBFA2T2, inhibits H3K27me3 demethylation and tumor growth by regulating metabolic genes and metabolite levels [RNA-seq]

Project description:Histone H3.1/3.2K27M and H3.3K27M mutation are driver mutations frequently identified in diffuse midline glioma (DMG). However, the precise mechanism by which H3K27M mediates tumorigenesis remains incompletely understood. By carrying out bait Protein-Protein Interaction followed by genome-wide screening (bPPI-seq) in H3.3WT and H3.3K27M mouse NSC models, we identified a novel histone reader CBFA2T2, which recognizes non-mutated or un-modified histone H3K27. Importantly, CBFA2T2 binding to H3K27, mediated by the NHR2 domain, is abrogated by the H3K27M oncogenic mutation. In H3.3 wildtype cells, CBFA2T2 represses transcription of genes involved in carbon metabolism and TCA cycle through its binding to H3K27. This alters the α-KG/Succinate (alpha-ketoglutarate/ Succinate) ratio and indirectly impacts H3K27me3 level, possibly through affecting the H3K27me3 demethylases. CBFA2T2 does not bind the H3.3K27M decorated chromatin in vivo, thus the K to M mutation, partially compromises the CBFA2T2 repressive function. However, over-expressing CBFA2T2 rescues the low H3K27me3 level in H3.3K27M mNSC and H3.3K27M DIPG cells, thus suppressing the H3.3K27M tumor growth. Our findings suggest a new mechanism, which may contribute to the low H3K27me3 level observed in the H3K27M cells, and provide a new strategy for H3K27M therapy through manipulation of CBFA2T2.

2026-04-22 | GSE277513 | GEO

A novel histone H3K27 reader, CBFA2T2, inhibits H3K27me3 demethylation and tumor growth by regulating metabolic genes and metabolite levels [ChIP-seq II]

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Expression data of PRDM14 overexpression in WT, Suz12 KO and Ctbp1/2 DKO ESCs

Project description:The pluripotency-associated transcriptional network is regulated by a core circuitry of transcription factors. The PR domain-containing protein, PRDM14, maintains pluripotency by activating and repressing transcription in a target gene-dependent manner. However, the mechanisms underlying dichotomic switching of PRDM14-mediated transcriptional control remains elusive. Here, we identified C-terminal binding protein 1/2 (CtBP1/2) as components of the PRDM14-mediated repressive complex. CtBP1/2 binding to PRDM14 depends on CBFA2T2, a core component of the PRDM14 complex. The loss of Ctbp1/2 impaired the PRDM14-mediated transcriptional repression required for pluripotency maintenance and primed to naïve pluripotency transition. Furthermore, CtBP1/2 also interacted with the PRC2 complexes, and the loss of Ctbp1/2 impaired the PRC2 and H3K27me3 enrichment at the target genes upon PRDM14 overexpression. These results suggest that evidence that the target gene-dependent transcriptional activity of PRDM14 is regulated by partner switching to ensure transition from primed to naïve pluripotency.

2020-07-15 | GSE134666 | GEO

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