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TBP in mitotic bookmarking and reactivation of transcription [ChIP-Seq]

ABSTRACT: TBP in mitotic bookmarking and reactivation of transcription [ChIP-Seq]

PROVIDER: PRJNA432433 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6660120_1.fastq.gz	Fastqsanger.gz
	SRR6660120_2.fastq.gz	Fastqsanger.gz
	SRR6660121_1.fastq.gz	Fastqsanger.gz
	SRR6660121_2.fastq.gz	Fastqsanger.gz
	SRR6660116_1.fastq.gz	Fastqsanger.gz

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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

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TBP in mitotic bookmarking and reactivation of transcription [ChIP-Seq]

Project description:To test of TBP binds in the same genomic regions in mitosis compared to interphase cells, we performed Chromatin ImmunoPrecipitation coupled with sequencing (ChIP-seq).

2018-07-04 | GSE109962 | GEO

Mitotic bookmarking by CTCF and fast post-mitotic gene reactivation in ES cells

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

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

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A stable mode of bookmarking by TBP recruits RNAPolymerase II to mitotic chromosomes

Project description:A stable mode of bookmarking by TBP recruits RNAPolymerase II to mitotic chromosomes

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TBP bookmarks and preserves neural stem cell fate memory by orchestrating local chromatin architecture [CUT&Tag]

Project description:Mitotic bookmarking has been posited as an important strategy for cells to faithfully propagate their fate memory though cell generations. However, the physiological significance and regulatory mechanisms of mitotic bookmarking in neural development remain unexplored. Here, we identified TBP (TATA binding protein) as a crucial mitotic bookmarker for preserving fate memory of Drosophila neural stem cells (NSCs). Phosphorylation by the super elongation complex (SEC) is important for TBP to retain as discrete foci at mitotic chromosomes of NSCs to effectively transmit their fate memory. TBP depletion leads to drastic NSC loss, whereas TBP overexpression enhances the ability of SEC to induce neural progenitor dedifferentiation and tumorigenesis. Importantly, TBP achieves its mitotic retention through recruiting the chromatin remodeler EP400, which in turn increases local chromatin accessibility via depositing H2A.Z. Thus, local chromatin remodeling ensures mitotic bookmarking, which may represent a general principle underlying the preservation of cell fate memory.

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TBP bookmarks and preserves neural stem cell fate memory by orchestrating local chromatin architecture [ATAC-seq]

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TBP bookmarks and preserves neural stem cell fate memory by orchestrating local chromatin architecture (RNA-Seq)

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TBP bookmarks and preserves neural stem cell fate memory by orchestrating local chromatin architecture (CUT&Tag)

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