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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [EU-RNA-seq]

ABSTRACT: Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [EU-RNA-seq]

PROVIDER: PRJNA592194 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10546860_1.fastq.gz	Fastqsanger.gz
	SRR10546860_2.fastq.gz	Fastqsanger.gz
	SRR10546861_1.fastq.gz	Fastqsanger.gz
	SRR10546861_2.fastq.gz	Fastqsanger.gz
	SRR10546862_1.fastq.gz	Fastqsanger.gz

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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [EU-RNA-seq]

Project description:During mitosis, transcription of genomic DNA is dramatically reduced, before its reactivation occurs during nuclear reformation in anaphase/telophase. Many aspects of the underlying principles that mediate transcriptional memory and reactivation in the daughter cells remain unclear. Here, we used ChIP-seq on synchronized cells at different stages after mitosis to generate genome-wide maps of histone modifications. In combination with EU-RNA-seq and Hi-C analyses, we show that, during prometaphase, promoters, enhancers, and insulators retain H3K4me3 and H3K4me1, while losing H3K27ac. Enhancers harboring mitotic H3K4me1 are associated with cell type-specific transcription factor motifs and mitotic activation of cell identity genes. As cells exit mitosis, promoters regain H3K27ac, which correlates with transcriptional reactivation. Insulators also gain H3K27ac and CCCTC binding factors (CTCF) in anaphase/telophase. This increase may play a role in the establishment of topologically associating domains (TADs). Together, our results show that the genome is reorganized in sequential order, in which histone methylations occur first in prometaphase, histone acetylation and CTCF in anaphase/telophase, transcription in cytokinesis, and long-range chromatin interactions in early G1. Our results provide insights into the histone modification landscape that allows faithful reestablishment of the transcriptional program and TADs during cell division.

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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [ChIP-seq]

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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [Hi-C]

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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation

Project description:Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation

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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [Hi-C]

Project description:Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [Hi-C]

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Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [ChIP-seq]

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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.

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Project description:The genome is thought to be transcriptionally silent during mitosis. Technical limitations have prevented the sensitive mapping of mitotic transcription and transcription reactivation during mitotic exit, and thus the networks by which transcriptome dynamics govern the generation of daughter cells have been unclear. We used 5-ethynyluridine to pulse-label intact transcripts during mitosis and mitotic exit and find that the first round of transcription activates genes that are involved in macromolecular synthesis, rather than cell identity. Many interphase genes exhibit residual transcription in mitosis, as confirmed by different methods of assessment, and a subset of genes are more highly transcribed in mitosis than in interphase. We suggest that mitotic transcription may serve an epigenetic function in restoring proper transcription patterns during mitotic exit.

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