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Cohesin removal reprograms mitotic gene expression upon mitotic entry

ABSTRACT: Cohesin removal reprograms mitotic gene expression upon mitotic entry

PROVIDER: PRJNA587151 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10386732_1.fastq.gz	Fastqsanger.gz
	SRR10386732_2.fastq.gz	Fastqsanger.gz
	SRR10386733_1.fastq.gz	Fastqsanger.gz
	SRR10386733_2.fastq.gz	Fastqsanger.gz
	SRR10386734_1.fastq.gz	Fastqsanger.gz

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Cohesin removal reprograms mitotic gene expression upon mitotic entry [ChIP-seq]

Project description:Cohesin removal reprograms mitotic gene expression upon mitotic entry [ChIP-seq]

| PRJNA587141 | ENA

Cohesin removal reprograms mitotic gene expression upon mitotic entry [RNA-seq I]

Project description:Cohesin removal reprograms mitotic gene expression upon mitotic entry [RNA-seq I]

| PRJNA540607 | ENA

Cohesin removal reprograms mitotic gene expression upon mitotic entry [RNA-seq II]

Project description:Cohesin removal reprograms mitotic gene expression upon mitotic entry [RNA-seq II]

| PRJNA587142 | ENA

Cohesin removal reprograms mitotic gene expression upon mitotic entry [ChIP-seq]

Project description:During mitosis, the genome is restructured to facilitate chromosome segregation, accompanied by dramatic changes in gene expression. However, the mechanisms that underlie mitotic transcriptional regulation are unclear. In contrast to transcribed genes, centromere regions retain transcriptionally active RNA Polymerase II (RNAPII) in mitosis. Here, we demonstrate that chromosome-localized cohesin is necessary and sufficient to retain active RNAPII on mitotic centromeres. Failure to remove cohesin from mitotic chromosome arms dramatically alters mitotic gene expression, and results in a failure to release elongating RNAPII and nascent transcripts from mitotic chromosomes. We propose that prophase cohesin removal is the key step in reprogramming gene expression as cells transition from G2 to mitosis, and is temporally coupled with chromosome condensation to coordinate chromosome segregation with changes in gene expression.

2020-01-30 | GSE139846 | GEO

Cohesin removal reprograms mitotic gene expression upon mitotic entry [RNA-seq II]

2020-01-30 | GSE139845 | GEO

Cohesin removal reprograms mitotic gene expression upon mitotic entry [RNA-seq I]

2020-01-30 | GSE130558 | GEO

Cohesin Removal Reprograms Gene Expression upon Mitotic Entry.

Project description:As cells enter mitosis, the genome is restructured to facilitate chromosome segregation, accompanied by dramatic changes in gene expression. However, the mechanisms that underlie mitotic transcriptional regulation are unclear. In contrast to transcribed genes, centromere regions retain transcriptionally active RNA polymerase II (Pol II) in mitosis. Here, we demonstrate that chromatin-bound cohesin is necessary to retain elongating Pol II at centromeres. We find that WAPL-mediated removal of cohesin from chromosome arms during prophase is required for the dissociation of Pol II and nascent transcripts, and failure of this process dramatically alters mitotic gene expression. Removal of cohesin/Pol II from chromosome arms in prophase is important for accurate chromosome segregation and normal activation of gene expression in G1. We propose that prophase cohesin removal is a key step in reprogramming gene expression as cells transition from G2 through mitosis to G1.

| S-EPMC7178822 | biostudies-literature

Cohesin removal reprograms mitotic gene expression upon mitotic entry

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-29 | GSE139856 | GEO

A Structure-Based Mechanism for DNA Entry into the Cohesin Ring

Project description:The ring-shaped cohesin complex is thought to fulfil its roles in sister chromatid cohesion, genome stability and gene regulation by topologically encircling DNAs. The ring is formed by two Structural Maintenance of Chromosome (SMC) subunits, whose ATPase heads are linked by a kleisin subunit. Additional components, including the Mis4Scc2/NIPL cohesin loader, engage the kleisin. Here, we visualize a DNA gripping intermediate during cohesin loading onto DNA by cryo-electron microscopy. ATP-dependent head engagement creates an interaction surface onto which Mis4Scc2/NIPL clamps the DNA. We use biophysical tools to establish the order of events during cohesin loading. DNA first traverses an N-terminal kleisin gate that was opened by ATP binding and closed again as the loader locks the DNA. Ensuing ATP hydrolysis and head disengagement, assisted by Mis4Scc2/NIPL, will complete DNA entry. A conserved kleisin N-terminal tail guides the DNA on its trajectory to successful topological DNA entry into the cohesin ring.

2020-08-05 | PXD018600 | Pride

The mitotic STAG3-cohesin defines male germline nucleome

Project description:Cohesin is a tetrameric protein complex with a ring-like structure that entraps DNA to ensure sister chromatid cohesion and higher-order chromatin organization. The mechanism by which cohesin regulates chromatin structure and gene expression remains a fundamental question. In multicellular organisms, germ cells are unique in that they tailor chromatin organization toward generating totipotency. As part of this program, spermatogonial stem cells (SSCs) in mammals, the source for male gametes, acquire distinctive chromatin organization with exceptionally weak insulation, but the underlying mechanism is unknown. Here, we show that STAG3, exclusively known to form meiotic cohesins, contributes to a mitotic cohesin defining nucleome programming during male germline development. With slower loop extrusion and shorter chromatin residence, STAG3–cohesin attenuates topologically associating domains (TADs) demarcated by CCCTC-binding factor (CTCF), re-wires both enhancer–promoter and Polycomb-mediated repressive interactions, and creates finer and strengthened compartments, establishing a characteristic SSC nucleome. Moreover, STAG3–cohesin controls the balance between SSC self-renewal and differentiation for spermatogenesis. Notably, mitotic STAG3–cohesin is also highly expressed in human B cells and potentially involved in B-cell malignancies. Thus, mitotic STAG3–cohesin with its unique loop extrusion property elucidates a principle for male germline nucleome programming and, more broadly, may contribute to human malignancy.

2025-07-07 | PXD045854 | JPOST Repository

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