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

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

PROVIDER: PRJNA909301 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22554731_1.fastq.gz	Fastqsanger.gz
	SRR22554731_2.fastq.gz	Fastqsanger.gz
	SRR22554732_1.fastq.gz	Fastqsanger.gz
	SRR22554732_2.fastq.gz	Fastqsanger.gz
	SRR22554733_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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Topoisomerase I (TOP1) is a functional mitotic interactor of the bookmarking factor HNF1B

Project description:HNF1B (Hepatocyte Nuclear Factor 1-Beta) is a POU-homeobox transcription factor expressed in kidney and frequently mutated in patients suffering from Congenital Anomalies of the Kidney and the Urinary Tract (CAKUT). HNF1B is a bookmarking factor, able to bind mitotic chromatin and necessary for the post-mitotic reactivation of gene expression. In order to characterize the molecular functions of HNF1B as a bookmarking factor, we performed ChIPseq on asynchronous and mitotic renal cells. We developed a novel ChIP method with a non-aqueous crosslinking (NAQC) to circumvent the well-known artefactual effects of formaldehyde crosslinking of mitotic chromosomes. NAQC-ChIP allowed the retention of the mitotic signal that was lost with a regular ChIP. With this novel methodology, we show that the vast majority HNF1B binding sites detected in asynchronous cells are also bound in mitosis.

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Topoisomerase I (TOP1) is a functional mitotic interactor of the bookmarking factor HNF1B [ChIPseq_786O]

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Topoisomerase I (TOP1) is a functional mitotic interactor of the bookmarking factor HNF1B [RNAseq_KEC]

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Topoisomerase I (TOP1) is a functional mitotic interactor of the bookmarking factor HNF1B [RNAseq_786O]

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Mitotic bookmarking redundancy by nuclear receptors in pluripotent cells.

Project description:Mitotic bookmarking transcription factors (TFs) are thought to mediate rapid and accurate reactivation after mitotic gene silencing. 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 biological significance and importance of their bookmarking function. Here we used targeted proteomics of the mitotic bookmarking TF ESRRB, an orphan nuclear receptor, to discover a large redundancy in mitotic binding among members of the protein super-family 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 those most efficiently reactivated in G1. 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.

| S-EPMC10948359 | biostudies-literature

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