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Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription [Histones]

ABSTRACT: Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription [Histones]

PROVIDER: PRJNA526633 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8713390.fastq.gz	Fastqsanger.gz
	SRR8713400.fastq.gz	Fastqsanger.gz
	SRR8713410.fastq.gz	Fastqsanger.gz
	SRR8713420.fastq.gz	Fastqsanger.gz
	SRR8713430.fastq.gz	Fastqsanger.gz

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Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription [Histones]

Project description:Global changes in chromatin organization and the cessation of transcription during mitosis are thought to challenge the resumption of appropriate transcription patterns following mitosis. The acetyl-lysine binding protein BRD4 has been previously suggested to function as a transcriptional “bookmark” on mitotic chromatin. Here, genome-wide location analysis of BRD4 in erythroid cells, combined with novel data normalization and peak characterization approaches, reveals that BRD4 widely occupies mitotic chromatin. However, removal of BRD4 from mitotic chromatin does not impair post-mitotic activation of transcription. Additionally, histone mass spectrometry reveals global preservation of most posttranslational modifications (PTMs) during mitosis. In particular, H3K14ac, H3K27ac, H3K122ac, and H4K16ac widely mark mitotic chromatin, especially at lineage-specific genes, and predict BRD4 mitotic binding genome wide. Therefore, BRD4 is likely not a mitotic bookmark but only a “passenger”. Instead, mitotic histone acetylation patterns may constitute the actual bookmarks that restore lineage-specific transcription patterns after mitosis.

2019-04-10 | GSE128161 | GEO

Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription

Project description:Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription

| PRJNA526632 | ENA

Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription [TFs]

Project description:Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription [TFs]

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Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription [TFs]

2019-04-10 | GSE128150 | GEO

Interrogating Histone Acetylation and BRD4 as Mitotic Bookmarks of Transcription.

Project description:Global changes in chromatin organization and the cessation of transcription during mitosis are thought to challenge the resumption of appropriate transcription patterns after mitosis. The acetyl-lysine binding protein BRD4 has been previously suggested to function as a transcriptional "bookmark" on mitotic chromatin. Here, genome-wide location analysis of BRD4 in erythroid cells, combined with data normalization and peak characterization approaches, reveals that BRD4 widely occupies mitotic chromatin. However, removal of BRD4 from mitotic chromatin does not impair post-mitotic activation of transcription. Additionally, histone mass spectrometry reveals global preservation of most posttranslational modifications (PTMs) during mitosis. In particular, H3K14ac, H3K27ac, H3K122ac, and H4K16ac widely mark mitotic chromatin, especially at lineage-specific genes, and predict BRD4 mitotic binding genome wide. Therefore, BRD4 is likely not a mitotic bookmark but only a "passenger." Instead, mitotic histone acetylation patterns may constitute the actual bookmarks that restore lineage-specific transcription patterns after mitosis.

| S-EPMC6664437 | biostudies-literature

Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription

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

2019-04-10 | GSE128162 | GEO

Mitotic post-translational modifications of histones promote chromatin compaction in vitro

Project description:As histones undergo major changes in their post-translational modifications during mitotic entry, we speculated that the spectrum of cell cycle-specific histone modifications might contribute to chromosome compaction during mitosis. To test this hypothesis, we isolated core histones from interphase and mitotic cells and reconstituted chromatin with them. We used mass spectrometry to show that key post-translational modifications remained intact during our isolation procedure.

2018-10-24 | PXD007116 | Pride

BRD4 marks chromatin on cell cycle genes activates their transcription and orchestrates mitotic cell division

Project description:BRD4 marks chromatin on cell cycle genes activates their transcription and orchestrates mitotic cell division

2022-01-31 | GSE153572 | GEO

BRD4 assists elongation of both coding and enhancer RNAs guided by histone acetylation

Project description:In serum-starved and re-fed mouse fibroblast, nascent RNA-seq analysis showed that the BET inhibitor JQ1 antagonized a process regulating PIC formation and a downstream process involved in progressive elongation. To specifically address the role of BRD4 and its interactions with acetylated histones and P-TEFb, YFP-tagged BRD4 proteins (wild type and mutant BRD4) were stably expressed in cells, endogenous BRD4 of which was knocked down by shRNA (shBRD4). Nascent RNA-seq analysis showed that BRD4 facilitated transcript elongation in a manner dependent on acetylated histone interaction but not P-TEFb. Furthermore, the role of BRD4 in enhancer activity was evaluated by mapping the intergenic distributions of Pol II, CDK9, H3K27 acetylation (Ac) and H4 Ac as well as BRD4 by ChIP-seq analysis. The results suggest that the role of intergenic BRD4 on nearby gene expression is mediated through enhanced synthesis of eRNA.

2014-11-10 | GSE58731 | GEO

Mitotic bookmarking by SWI/SNF subunits

Project description:For cells to initiate and sustain a differentiated state, it is necessary that a “memory” of this state is transmitted through mitosis to the daughter cells. Mammalian SWItch/ Sucrose Non- Fermentable (SWI/SNF) complexes, also called Brg1/ Brg- associated factors (BAF), control cell identity by modulating chromatin architecture to regulate gene expression, but whether they participate in cell fate memory is unclear. Here, we provide evidence that subunits of SWI/SNF act as mitotic bookmarks to safeguard cell identity during cell division. The SWI/SNF core subunits SMARCE1 and SMARCB1 are displaced from enhancers but bound on promoters during mitosis and we show that this binding is required for appropriate reactivation of bound genes after mitotic exit. Ablation of SMARCE1 during a single mitosis in mouse embryonic stem cells is sufficient to disrupt gene expression, impair the occupancy of several established bookmarks at a subset of their targets, and cause aberrant neural differentiation. Thus, SWI/SNF subunit SMARCE1 plays a mitotic bookmarking role and is essential for heritable epigenetic fidelity during transcriptional reprogramming.

2023-03-18 | GSE189563 | GEO

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