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

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

PROVIDER: PRJNA526569 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8712440.fastq.gz	Fastqsanger.gz
	SRR8712441.fastq.gz	Fastqsanger.gz
	SRR8712432.fastq.gz	Fastqsanger.gz
	SRR8712442.fastq.gz	Fastqsanger.gz
	SRR8712433.fastq.gz	Fastqsanger.gz

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

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 | GSE128150 | 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 [Histones]

2019-04-10 | GSE128161 | GEO

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

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

| PRJNA526633 | ENA

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

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

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

Mitotic bookmarking redundancy by nuclear receptors mediates robust post-mitotic reactivation of the pluripotency network.

Project description:Mitotic bookmarking transcription factors (TFs) are thought to mediate rapid and accurate post-mitotic gene reactivation. However, the loss of individual bookmarking TFs often leads to the deregulation of only a small proportion of their mitotic targets, raising doubts on the significance and importance of their bookmarking function. Here, we used targeted proteomics of the mitotic bookmarking TF ESRRB, an orphan nuclear receptor, to discover an unexpected redundancy among members of the protein superfamily of nuclear receptors. Focusing on the nuclear receptor NR5A2, which together with ESRRB is essential in maintaining pluripotency in mouse embryonic stem cells, we demonstrate conjoint bookmarking activity of both factors on promoters and enhancers of a large fraction of active genes, particularly the most rapidly and strongly reactivated ones. Upon fast and simultaneous degradation of both factors during mitotic exit, hundreds of mitotic targets of ESRRB/NR5A2, including key players of the pluripotency network, display attenuated transcriptional reactivation. We propose that redundancy in mitotic bookmarking TFs, especially nuclear receptors, confers robustness to the reestablishment of gene regulatory networks after mitosis.

2023-11-20 | PXD038950 | Pride

Mitotic bookmarking redundancy by nuclear receptors mediates robust post-mitotic reactivation of the pluripotency network

2022-12-06 | GSE220253 | GEO