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Coordination of widespread transcription at enhancers and target genes through BRD4 (His-NET-Seq)

ABSTRACT: Coordination of widespread transcription at enhancers and target genes through BRD4 (His-NET-Seq)

PROVIDER: PRJNA886066 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21776478.fastq.gz	Fastqsanger.gz
	SRR21776479.fastq.gz	Fastqsanger.gz
	SRR21776480.fastq.gz	Fastqsanger.gz
	SRR21776481.fastq.gz	Fastqsanger.gz
	SRR21776482.fastq.gz	Fastqsanger.gz

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Similar Datasets

Coordination of widespread transcription at enhancers and target genes through BRD4 (His-NET-Seq)

Project description:Gene transcription by RNA polymerase II (Pol II) is under the control of promoters and distal regulatory elements known as enhancers. Enhancers are themselves transcribed by Pol II which correlates with their activity. How enhancer transcription is regulated and coordinated with transcription at target genes has remained unclear. Here, we developed a high-sensitive native elongating transcript sequencing approach, called HiS-NET-seq, to provide an extended high-resolution view on transcription, especially at lowly transcribed regions such as enhancers. HiS-NET-seq uncovers new transcriptional enhancers in human cells. An integrated multi-omics analysis shows that transcription at most enhancers depends on the BET protein BRD4. We provide evidence for a direct BRD4-mediated coupling of Pol II transcription at enhancers and target genes. Specifically, BRD4 links elongation activation at enhancers and genes by maintaining their proximity. These studies reveal that transcription at enhancers and target genes is coordinated at the level of elongation.

2023-07-06 | GSE214593 | GEO

Coordination of widespread transcription at enhancers and target genes through BRD4 (HiChIP)

2023-07-06 | GSE214591 | GEO

Coordination of widespread transcription at enhancers and target genes through BRD4 (ChIP-Rx)

2023-07-06 | GSE214590 | GEO

Coordination of widespread transcription at enhancers and target genes through BRD4

Project description:Coordination of widespread transcription at enhancers and target genes through BRD4

| PRJNA886064 | ENA

Coordination of widespread transcription at enhancers and target genes through BRD4 (HiChIP)

Project description:Coordination of widespread transcription at enhancers and target genes through BRD4 (HiChIP)

| PRJNA886067 | ENA

Coordination of widespread transcription at enhancers and target genes through BRD4 (ChIP-Rx)

Project description:Coordination of widespread transcription at enhancers and target genes through BRD4 (ChIP-Rx)

| PRJNA886065 | ENA

HIS susceptibility in Swiss pigs

Project description:HIS susceptibility in Swiss pigs

| PRJEB62539 | ENA

Net Cleaning

Project description:Net Cleaning Raw sequence reads

| PRJNA930680 | ENA

A BRD4-mediated elongation control point primes transcribing RNA polymerase II for 3'-processing and termination [NET-seq]

Project description:In this study, we reveal that BRD4 underlies a general 5'-elongation checkpoint that primes transcribing RNA polymerase II for 3'-RNA processing and transcription termination. BRD4-specific degradation impairs Pol II pause release, induces massive readthrough transcription, and RNA cleavage defects. Acute loss of BRD4 disrupts the recruitment of 3'-RNA processing factors.

2021-07-30 | GSE158963 | GEO

Genome-wide BRD4, PolII and p65 occupancy as well as chromatin modifications in bone marrow derived macrophages from BRD4 conditional KO mice

Project description:We are reporting here genome wide distribution of BRD4 in bone marrow derived macrophages at steady state level and in reponse to LPS stimulation. In both condition, BRD4 distribution was found to be widespread in intragenic as well as intergenic regions with enrichment specifically near TSS. Characteristically BRD4 signal were highly enriched on enhancers of some active genes and hence were classified as BRD4 rich super-enhancers (>12kb long stretches). Super-enhancers are formed, in some instances by redistribution of BRD4 on LPS stimulated genes. BRD4 binding well correlated PolII binding at the chromatin acetylated at H3K27, H3K9 and H4tetraK. Interestingly many LPS induced BRD4 independent genes, despite BRD4 loss in the KO, maintained PolII binding at the chromatin enriched with acetylated lysines at H3K27, H3K9 and H4tetraK. Additionally among some BRD4 independent LPS inducible genes we detected stronger p65 enrichment in the KO. In contrast, P65 binding was not detected in BRD4 dependent genes. These observations provided evidence of plasticity of epigenetic changes in retaining inflammatory reponses in macrophages.

2019-02-21 | GSE113226 | GEO

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