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

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

PROVIDER: PRJNA643257 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12121473.fastq.gz	Fastqsanger.gz
	SRR12121474.fastq.gz	Fastqsanger.gz
	SRR12121475.fastq.gz	Fastqsanger.gz
	SRR12121476.fastq.gz	Fastqsanger.gz
	SRR12121477.fastq.gz	Fastqsanger.gz

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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

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 [TFs]

2019-04-10 | GSE128150 | GEO

Chip-seq mapping of active chromatin marks in BRD4-NUT and different NMC cells

Project description:BRD4-NUT megadomains is an order of magnitude larger than super-enhancer regions and displays a more continuously enriched profile rather than appearing as a cluster of individual peaks. Chip-seq mapping of active chromatin marks in BRD4-NUT and different NMC cells

2015-07-14 | E-GEOD-70870 | biostudies-arrayexpress

Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription

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

| PRJNA526632 | ENA

BRD4 orchestrates genome folding to promote neural crest progenitor differentiation

Project description:BRD4 orchestrates genome folding to promote neural crest progenitor differentiation

| PRJNA716975 | ENA

Brd4 marks select genes on mitotic chromatin and directs postmitotic transcription.

Project description:On entry into mitosis, many transcription factors dissociate from chromatin, resulting in global transcriptional shutdown. During mitosis, some genes are marked to ensure the inheritance of their expression in the next generation of cells. The nature of mitotic gene marking, however, has been obscure. Brd4 is a double bromodomain protein that localizes to chromosomes during mitosis and is implicated in holding mitotic memory. In interphase, Brd4 interacts with P-TEFb and functions as a global transcriptional coactivator. We found that throughout mitosis, Brd4 remained bound to the transcription start sites of many M/G1 genes that are programmed to be expressed at the end of, or immediately after mitosis. In contrast, Brd4 did not bind to genes that are expressed at later phases of cell cycle. Brd4 binding to M/G1 genes increased at telophase, the end phase of mitosis, coinciding with increased acetylation of histone H3 and H4 in these genes. Increased Brd4 binding was accompanied by the recruitment of P-TEFb and de novo M/G1 gene transcription, the events impaired in Brd4 knockdown cells. In sum, Brd4 marks M/G1 genes for transcriptional memory during mitosis, and upon exiting mitosis, this mark acts as a signal for initiating their prompt transcription in daughter cells.

| S-EPMC2785733 | biostudies-literature

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 [TFs]

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

| PRJNA526569 | ENA

FAM83D directs protein kinase CK1α to the mitotic spindle for proper spindle positioning

Project description:The concerted action of many protein kinases helps orchestrate the error-free progression through mitosis of mammalian cells. The roles and regulation of some prominent mitotic kinases, such as cyclin-dependent kinases, are well-established. However, these and other known mitotic kinases alone cannot account for the extent of protein phosphorylation that has been reported during mammalian mitosis. Here we demonstrate that CK1α, of the casein kinase 1 family of protein kinases, localises to the spindle and is required for proper spindle-positioning and timely cell division. CK1α is recruited to the spindle by FAM83D, and cells devoid of FAM83D, or those harbouring CK1α-binding-deficient FAM83DF283A/F283A knockin mutation, display pronounced spindle-positioning defects, and a prolonged mitosis. Restoring FAM83D at the endogenous locus in FAM83D-/- cells, or artificially delivering CK1α to the spindle in FAM83DF283A/F283A cells, rescues these defects. These findings implicate CK1α as new mitotic kinase that orchestrates the kinetics and orientation of cell division.

2019-07-15 | PXD013808 | Pride

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