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Histone deactylase 3 controls a transcriptional network required for B cell maturation [PRO-seq]

ABSTRACT: Histone deactylase 3 controls a transcriptional network required for B cell maturation [PRO-seq]

PROVIDER: PRJNA540500 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8992360.fastq.gz	Fastqsanger.gz
	SRR8992361.fastq.gz	Fastqsanger.gz
	SRR8992362.fastq.gz	Fastqsanger.gz
	SRR8992363.fastq.gz	Fastqsanger.gz
	SRR8992364.fastq.gz	Fastqsanger.gz

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Histone deactylase 3 controls a transcriptional network required for B cell maturation

Project description:Histone deactylase 3 controls a transcriptional network required for B cell maturation

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Histone deactylase 3 controls a transcriptional network required for B cell maturation [ChIP-seq]

Project description:Histone deactylase 3 controls a transcriptional network required for B cell maturation [ChIP-seq]

| PRJNA540526 | ENA

Histone deactylase 3 controls a transcriptional network required for B cell maturation [PRO-seq]

Project description:We used Cd19-Cre to conditionally delete Hdac3 in order to define its role in germinal center B cells, which represent the cell of origin for many B cell malignancies. Cd19-Cre-Hdac3-/- mice showed impaired germinal center (GC) formation along with a defect in plasmablast generation. Analysis of Hdac3-/- GCs revealed a reduction in dark zone centroblasts and accumulation of light zone centrocytes. RNA-seq revealed a significant correlation between genes up-regulated upon Hdac3 loss and those up-regulated in Foxo1-deleted GC B cells, even though Foxo1 typically activates transcription. Therefore, to determine whether gene expression changes observed in Hdac3-/- GCs were a result of direct effects of Hdac3 deacetylase activity on transcription, we used an HDAC3 selective inhibitor to examine nascent transcription in germinal center-derived cell lines. Transcriptional changes upon HDAC3 inhibition in cells highly correlated with transcriptional changes observed in GCs in vivo. Further comparison of PRO-seq data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac identified direct targets of HDAC3 function including CD86, CD83 and CXCR5 that are likely responsible for driving the light zone phenotype observed in vivo.

2019-09-12 | GSE130502 | GEO

Histone deacetylase 3 controls a transcriptional network required for B cell maturation.

Project description:Histone deacetylase 3 (Hdac3) is a target of the FDA approved HDAC inhibitors, which are used for the treatment of lymphoid malignancies. Here, we used Cd19-Cre to conditionally delete Hdac3 to define its role in germinal center B cells, which represent the cell of origin for many B cell malignancies. Cd19-Cre-Hdac3-/- mice showed impaired germinal center formation along with a defect in plasmablast production. Analysis of Hdac3-/- germinal centers revealed a reduction in dark zone centroblasts and accumulation of light zone centrocytes. RNA-seq revealed a significant correlation between genes up-regulated upon Hdac3 loss and those up-regulated in Foxo1-deleted germinal center B cells, even though Foxo1 typically activates transcription. Therefore, to determine whether gene expression changes observed in Hdac3-/- germinal centers were a result of direct effects of Hdac3 deacetylase activity, we used an HDAC3 selective inhibitor and examined nascent transcription in germinal center-derived cell lines. Transcriptional changes upon HDAC3 inhibition were enriched for light zone gene signatures as observed in germinal centers. Further comparison of PRO-seq data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac identified direct targets of HDAC3 function including CD86, CD83 and CXCR5 that are likely responsible for driving the light zone phenotype observed in vivo.

| S-EPMC6847391 | biostudies-literature

Histone deactylase 3 controls a transcriptional network required for B cell maturation [ChIP-seq]

2019-09-12 | GSE130516 | GEO

Histone deactylase 3 controls a transcriptional network required for B cell maturation

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

2019-09-12 | GSE130529 | GEO

Transcriptional coactivator MED15 is required for beta cell maturation

Project description:Transcriptional coactivator MED15 is required for beta cell maturation

| PRJNA564631 | ENA

Ptbp2 controls an alternative splicing network required for cell communication during spermatogenesis

Project description:Ptbp2 controls an alternative splicing network required for cell communication during spermatogenesis

| PRJNA314953 | ENA

MEMO1 is required for ameloblast maturation and functional enamel formation

Project description:MEMO1 is required for ameloblast maturation and functional enamel formation

| PRJNA987732 | ENA

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

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