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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 [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 [Histones]

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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

The CIP2A-TOPBP1 axis orchestrates mitotic DNA repair

Project description:DNA double-strand breaks (DSBs) accumulate in mitosis in response to DNA replication stress or deficiency in breast cancer susceptibility type 1 and 2 (BRCA1/2). This is a critical threat to genome stability as the classical DSB repair pathways non-homologous end joining (NHEJ) and homologous recombination (HR) are repressed(1-7). Instead, mitotic repair relies on the processes of microhomology-mediated end joining (MMEJ) or mitotic DNA synthesis (MiDAS), but how these pathways are coordinated and regulated remains unclear.  Here, we reveal that the CIP2A-TOPBP1 axis orchestrates DSB repair in mitosis by promoting CDK1-driven phosphorylation of SLX4 at Thr1260, recruiting the SMX complex to promote MiDAS. In addition, the CIP2A-TOPBP1 axis regulates mitotic Polθ recruitment and MMEJ. This dual mechanism ensures coordinated DSBs repair by integrating spatial control of TOPBP1-CIP2A chromatin recruitment with the temporal regulation provided by mitotic kinases, thereby preserving genome stability. These findings provide new insights into DSB repair dynamics in mitosis and offer a mechanistic rationale for the synthetic lethality of CIP2A in BRCA1/2-deficient tumors through the simultaneous impairment of break induced replication (BIR)-like MiDAS and MMEJ, which are genetically redundant pathways to HR.

2025-09-19 | PXD068371 | Pride

Interrogating histone acetylation and BRD4 as mitotic bookmarks of transcription

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

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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.

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BRD4 orchestrates genome folding to promote neural crest progenitor differentiation

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

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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 [Histones]

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

| PRJNA526633 | ENA