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Histone Deacetylases (HDACs) are essential for transcription of the pluripotent network in embryonic stem cells [Pro-Seq]

ABSTRACT: Histone Deacetylases (HDACs) are essential for transcription of the pluripotent network in embryonic stem cells [Pro-Seq]

PROVIDER: PRJNA563879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10067473.fastq.gz	Fastqsanger.gz
	SRR10067474.fastq.gz	Fastqsanger.gz
	SRR10067475.fastq.gz	Fastqsanger.gz
	SRR10067476.fastq.gz	Fastqsanger.gz
	SRR10067477.fastq.gz	Fastqsanger.gz

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Similar Datasets

Histone Deacetylases (HDACs) are essential for transcription of the pluripotent network in embryonic stem cells [Pro-Seq]

Project description:Histone acetylation is a dynamic modification regulated by the opposing actions of histone acetyltransferases and histone deacetylases (HDACs). Deacetylation of histone tails results in chromatin tightening and therefore HDACs are generally regarded as transcriptional repressors. Counterintuitively, simultaneous deletion of HDAC1 and HDAC2 in embryonic stem cells (ESC) reduced expression of pluripotent transcription factors, Oct4, Sox2 and Nanog (OSN). By shaping global histone acetylation HDACs indirectly regulate the activity of acetyl-lysine readers, such as BRD4. To examine the direct effects of HDAC (LBH589) and BRD4 (JQ1) inhibition on the ESC transcriptome, we performed precision nuclear run-on and sequencing (PRO-seq) analysis. Both LBH589 and JQ1 caused a marked reduction in the pluripotent network. However, while JQ1 treatment induced widespread transcriptional pausing of genes, HDAC inhibition caused a reduction in both paused and elongating polymerase, suggesting an overall reduction in recruitment of RNAPII. Using enhancer RNA (eRNA) expression to measure enhancer activity, we found that while HDAC activity regulates fewer enhancers than JQ1, LBH589 sensitive eRNAs were preferentially associated with super-enhancers and OSN binding sites. These findings suggest that HDAC activity is required for maintenance of pluripotency by regulating the OSN enhancer network via optimal recruitment of RNA polymerase II.

2020-08-01 | GSE136860 | GEO

Histone Deacetylases (HDACs) are essential for transcription of the pluripotent network in embryonic stem cells

Project description:Histone Deacetylases (HDACs) are essential for transcription of the pluripotent network in embryonic stem cells

| PRJNA562875 | ENA

Histone Deacetylases (HDACs) are essential for transcription of the pluripotent network in embryonic stem cells

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

2020-08-01 | GSE136621 | GEO

Genome-wide mapping of HATs and HDACs in human CD4+ T cells

2009-08-20 | GSE15735 | GEO

Genome-wide mapping of HATs and HDACs in human CD4+ T cells

Project description:Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and ﬁnd that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs. high throughput sequencing: genome-wide analysis of 5 HATs, 4 HDACs in human CD4+ cells, Tip60 and HDAC6 in activated CD4 cells, genome-wide analysis of 2 histone acetylations and RNA Polymerase II after HDAC inhibitor treatment in CD4, histone modification with WDR5 knock-down and HDAC inhibitor treatment in HeLa cells expression profiling: Global change in gene expression in human CD4+ T cells after HDAC inhibitor treatment for 2hours and 12 hours. (9 samples in total)

2009-08-20 | E-GEOD-15735 | biostudies-arrayexpress

A Redox-Dependent Pathway for Regulating Reversible HDACs Synchronizes Crown Root Development in Rice

Project description:As a signal molecular in aerobic organism, how reactive oxygen species (ROS) regulates normal life is a fundamental biological question. Locally accumulated ROS have been reported to balance cell division and differentiation in root apical meristem. However, the underlying molecular mechanism is unclear. Here, we reveal that developmentally produced H2O2 in plant root apical meristem (RAM) triggers reversible acetylation modification of proteins which involved in protein synthesis and cell proliferation. WOX11, an essential transcription factor for crown roots (CRs) formation, modulates ROS homeostasis by directly regulating class III peroxidases. HDACs (histone deacetylases) sense cellular redox status to enhance their enzyme activities, which drives protein acetylation level alterations in rice roots. Oxidation-dependent on WOX11 triggered protein acetylation modification leads to a robust root system in rice. Our study revealed a novel regulatory mechanism which cellular redox status via a WOX11-dependent manner regulates protein acetylation during rice crown root development. The molecular link between the redox status and HDACs activities through WOX11-dependent pathway may provide new insight into which plants exploit developmentally produced ROS to direct organogenesis. Additionally, HDACs reversible enzyme activity via redox-regulated endows with the flexibility of protein modification control in dealing with developmental and changing environmental cues.

2022-08-10 | PXD029260 | Pride

Histone Deacetylases (HDACs) maintain expression of the pluripotent gene network via recruitment of RNA polymerase II to coding and non-coding loci.

Project description: Not available

| S-EPMC10104071 | biostudies-literature

HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors

Project description:In S. cerevisiae, replication timing is controlled by epigenetic mechanisms restricting the accessibility of origins to limiting initiation factors. About 30% of these origins are located within repetitive DNA sequences such as the ribosomal DNA (rDNA) array, but their regulation is poorly understood. Here, we have investigated how histone deacetylases (HDACs) control the replication program in budding yeast. This analysis revealed that two HDACs, Rpd3 and Sir2, control replication timing in an opposite manner. Whereas Rpd3 delays initiation at late origins, Sir2 is required for the timely activation of early origins. Moreover, Sir2 represses initiation at rDNA origins whereas Rpd3 counteracts this effect. Remarkably, deletion of SIR2 restored normal replication in rpd3 cells by reactivating rDNA origins. Together, these data indicate that HDACs control the replication timing program in budding yeast by modulating the ability of repeated origins to compete with single-copy origins for limiting initiation factors. BrdU-IP-chip analysis of origin usage in different yeast HDAC mutants

2014-03-26 | E-GEOD-56171 | biostudies-arrayexpress

Novel Azaborine-Based Inhibitors of Histone Deacetylases (HDACs).

Project description: Not available

| S-EPMC12525784 | biostudies-literature

EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent

Project description:In proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PCR2 writing of H3K27me3 is mechanistically required for gene silencing. Here we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (Embryonic Ectoderm Development) inactivation in the postnatal heart (Eed CKO ) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in Eed CKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized Eed CKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.

2017-04-14 | GSE73771 | GEO

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