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A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells. [ChIP-seq]

ABSTRACT: A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells. [ChIP-seq]

PROVIDER: PRJNA1036385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26685747.fastq.gz	Fastqsanger.gz
	SRR26685748.fastq.gz	Fastqsanger.gz
	SRR26685749.fastq.gz	Fastqsanger.gz

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Similar Datasets

A CHD8-TRRAP axis facilitates MYC- and E2F-target gene regulation in human neural stem cells.

Project description:Mutations in ATP-dependent chromatin remodeler CHD8 cause one of the most frequent monogenetic forms of autism and also associate with brain overgrowth. Nevertheless, activities of CHD8 in autism-relevant cell types are still poorly understood. Here we purify the CHD8 protein from human neural stem cells and determine its interaction partners by mass spectrometry. We identify the TRRAP-complex, a coactivator of MYC and E2F transcription factors, as a prominent CHD8 interaction partner. CHD8 colocalizes genome-wide with TRRAP and TRRAP and CHD8 bind together to MYC- and E2F-target gene promoters in human neural stem cells. Acute depletion of CHD8 or TRRAP from human neural stem cells shows down-regulation of MYC- and E2F-target genes as most prominent gene-regulatory events. MYC and E2F factors are established oncogenes known to regulate cell growth. Our results link CHD8 to TRRAP in facilitating regulation of MYC- and E2F-target genes in neural stem cells.

2025-05-06 | PXD044582 | Pride

A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells. [ChIP-seq]

Project description:Mutations in ATP-dependent chromatin remodeler CHD8 cause one of the most frequent monogenetic forms of autism and is associated with brain overgrowth. Nevertheless, the activities of CHD8 in autism-relevant cell types are still poorly understood. Here, we purify the CHD8 protein from human neural stem cells and determine its interaction partners using mass spectrometry. We identify the TRRAP complex, a coactivator of MYC and E2F transcription factors, as a prominent CHD8 interaction partner. CHD8 colocalizes genome-wide with TRRAP and bind together at MYC and E2F target gene promoters in human neural stem cells. Depletion of CHD8 or TRRAP in human neural stem cells shows downregulation of MYC and E2F target genes as the most prominent gene-regulatory events. MYC and E2F transcription factors are established oncogenes known to regulate cell growth. Our results link CHD8 to TRRAP and suggest they act together in facilitating the regulation of MYC and E2F target genes in neural stem cells.

2024-11-06 | GSE247132 | GEO

A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells. [RNA-Seq]

2024-11-06 | GSE247131 | GEO

A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells.

Project description:A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells.

| PRJNA1036257 | ENA

A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells. [RNA-Seq]

Project description:A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells. [RNA-Seq]

| PRJNA1036386 | ENA

A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells.

Project description:Mutations in ATP-dependent chromatin remodeler CHD8 cause one of the most frequent monogenetic forms of autism and are associated with brain overgrowth. Nevertheless, the activities of CHD8 in autism-relevant cell types are still poorly understood. Here, we purify the CHD8 protein from human neural stem cells and determine its interaction partners using mass spectrometry. We identify the TRRAP complex, a coactivator of MYC and E2F transcription factors, as a prominent CHD8 interaction partner. CHD8 colocalizes genome-wide with TRRAP and binds together at MYC and E2F target gene promoters in human neural stem cells. Depletion of CHD8 or TRRAP in human neural stem cells shows downregulation of MYC and E2F target genes as the most prominent gene-regulatory events. Depletion of CHD8 diminishes cell-cycle entry into S-phase. MYC and E2F transcription factors are established oncogenes and regulate cell growth. Our results link CHD8 to TRRAP in facilitating the regulation of MYC and E2F target genes in human neural stem cells.

| S-EPMC11914185 | biostudies-literature

A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells.

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

2024-11-06 | GSE247133 | GEO

Cell cycle dependence of neuroprogenitor fate determination regulated by Trrap-mediated histone acetylation

Project description:Epigenetic control of neural stem/progenitor cell fate is fundamental to achieve a fully brain architecture. Two intrinsic programs regulate neurogenesis, one by epigenetic-mediated gene transcription and another by cell cycle control. Whether and how these two are coordinated to determine temporally and spatially neural development remains unknown. Here we show that deletion of Trrap (Transcription translation associated protein), an essential cofactor for HAT (histone acetyltransferase), leads to severe brain atrophy due to a combination of cell death and a blockade of neuron production. Specifically, Trrap deletion forces differentiation of apical progenitor (AP) fate into basal progenitors (BP) and neurons thereby limiting the total neurogenic production. Despite TrrapM-bM-^@M-^Ys general role in transcriptional regulation, a genome-wide transcriptome analysis of neuroprogenitors identified the cell cycle regulators that are specifically affected by Trrap deletion. Furthermore, E2F-dependent recruitment of HAT and transcription factors to the promoter of cell cycle regulators is impaired in Trrap-deleted neuroprogenitors. Consistent with these molecular changes, Trrap deletion lengthens particularly G1 and S phases in APs in vivo. Therefore, our study reveals an essential and a distinct function of Trrap-HAT in regulation of cell cycle progression that is required for proper determination of neuroprogenitor fate. Determine gene transcriptions by comparing Trrap-deleted and wild type samples

2014-05-01 | E-GEOD-43650 | biostudies-arrayexpress

Cell cycle dependence of neuroprogenitor fate determination regulated by Trrap-mediated histone acetylation

Project description:Epigenetic control of neural stem/progenitor cell fate is fundamental to achieve a fully brain architecture. Two intrinsic programs regulate neurogenesis, one by epigenetic-mediated gene transcription and another by cell cycle control. Whether and how these two are coordinated to determine temporally and spatially neural development remains unknown. Here we show that deletion of Trrap (Transcription translation associated protein), an essential cofactor for HAT (histone acetyltransferase), leads to severe brain atrophy due to a combination of cell death and a blockade of neuron production. Specifically, Trrap deletion forces differentiation of apical progenitor (AP) fate into basal progenitors (BP) and neurons thereby limiting the total neurogenic production. Despite Trrap’s general role in transcriptional regulation, a genome-wide transcriptome analysis of neuroprogenitors identified the cell cycle regulators that are specifically affected by Trrap deletion. Furthermore, E2F-dependent recruitment of HAT and transcription factors to the promoter of cell cycle regulators is impaired in Trrap-deleted neuroprogenitors. Consistent with these molecular changes, Trrap deletion lengthens particularly G1 and S phases in APs in vivo. Therefore, our study reveals an essential and a distinct function of Trrap-HAT in regulation of cell cycle progression that is required for proper determination of neuroprogenitor fate.

2014-05-01 | GSE43650 | GEO

Epstein-Barr Virus facilitates KLF14 expression by regulating the cooperative binding of E2F-Rb-HDAC in latent infection

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