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The length and strength of compartmental interactions are modulated by condensin II activity [RNA-Seq]

ABSTRACT: The length and strength of compartmental interactions are modulated by condensin II activity [RNA-Seq]

PROVIDER: PRJNA1012304 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27955153_1.fastq.gz	Fastqsanger.gz
	SRR27955153_2.fastq.gz	Fastqsanger.gz
	SRR27955154_1.fastq.gz	Fastqsanger.gz
	SRR27955154_2.fastq.gz	Fastqsanger.gz
	SRR27955155_1.fastq.gz	Fastqsanger.gz

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The length and strength of compartmental interactions are modulated by condensin II activity

Project description:The length and strength of compartmental interactions are modulated by condensin II activity

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The length and strength of compartmental interactions are modulated by condensin II activity [Hi-C]

Project description:The length and strength of compartmental interactions are modulated by condensin II activity [Hi-C]

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The length and strength of compartmental interactions are modulated by condensin II activity [RNA-Seq]

Project description:Condensin II plays a crucial role in shaping chromosome structure throughout the cell cycle, but its specific functions during interphase have remained unclear. In this study, we utilized Oligopaints and Hi-C techniques to investigate how changes in condensin II levels affect chromosome organization across various length scales. Our findings reveal that condensin II has a significant impact on long-range interactions within chromosomes, which are essential for the organization of intrachromosomal compartments. Importantly, these effects occur independently of the chromatin state. Furthermore, overexpression of condensin II during interphase leads to the formation of "peri-centric super stripes" observed through Hi-C analysis, indicating a disruption of the boundary between heterochromatin and euchromatin on Drosophila chromosomes. Collectively, our results challenge the existing belief that compartments form without the involvement of a loop extruder and suggest that condensin II activity is a prerequisite for driving proximity between distal compartmental domains within chromosomes.

2023-09-03 | GSE242223 | GEO

The length and strength of compartmental interactions are modulated by condensin II activity [Hi-C]

2023-09-03 | GSE242222 | GEO

The length and strength of compartmental interactions are modulated by condensin II activity

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

2023-09-03 | GSE242224 | GEO

Involvement of Condensin in Cellular Senescence through Gene Regulation and Compartmental Reorganization

Project description:Cellular senescence is a state of stable cell growth arrest induced by various stimuli such as oncogene expression and telomere shortening, referred to as oncogene-induced senescence (OIS) and replicative senescence (RS), respectively. Senescence is accompanied not only by global transcriptional alterations but also by 3D genome reorganization. Here we demonstrate that the human condensin II complex participates in cellular senescence via gene regulation and reorganization of euchromatic A and heterochromatic B chromatin compartments. OIS and RS are accompanied by A-to-B and B-to-A compartmental transitions, the latter of which occur more frequently and account for 15% of the human genome. Mechanistically, condensin is enriched at A compartments, especially at gene promoters and typical/super enhancers, and implicated in the B-to-A transitions. Genes present at B-to-A-switching regions tend to be up-regulated. The full activation of senescence genes (SASP genes and p53 targets) requires condensin; its depletion impairs senescence markers such as the activity of senescence-associated beta-galactosidase (SA-beta-gal) and senescence-associated heterochromatic foci (SAHF). This study describes that condensin reinforces euchromatic A compartments and is required for optimal expression of senescence genes, thereby contributing to the establishment and maintenance of the senescent state.

2019-11-06 | GSE118494 | GEO

Involvement of Condensin in Cellular Senescence through Gene Regulation and Compartmental Reorganization

Project description:Involvement of Condensin in Cellular Senescence through Gene Regulation and Compartmental Reorganization

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Condensin II Counters Cohesin and RNA Polymerase II in 3D Chromatin Organization

Project description:CTCF is present at the anchors of thousands of loops likely formed via cohesin-mediated loop extrusion in mammalian cells. Interaction domains present in D. melanogaster chromosomes form via the segregation of active and inactive chromatin in the absence of CTCF looping, but the role of transcription versus other architectural proteins in chromatin organization is unclear. Here we find that positioning of RNAPII via transcription elongation is essential in the formation of gene loops, which in turn interact to form compartmental domains. Inhibition of transcription elongation or depletion of cohesin decreases gene looping and formation of active compartmental domains. In contrast, depletion of condensin II, which also localizes to active chromatin, results in increased gene looping, formation of compartmental domains, and stronger intra-chromosomal compartmental interactions. Condensin II has a similar role in maintaining inter-chromosomal interactions responsible for pairing between homologous chromosomes, whereas inhibition of transcription elongation or cohesin depletion has little effect on homolog pairing. The results suggest distinct roles for cohesin and condensin II in the establishment of 3D nuclear organization in Drosophila.

2019-03-11 | GSE118756 | GEO

DNA break formation induces Scc2/cohesin-dependent recruitment of condensin to meiotic chromosomes

Project description:Meiotic chromosome pairing, recombination, and fertility depends on the conserved loop-axis architecture of meiotic chromosomes. This architecture is modulated by condensin, a structural maintenance of chromosome (SMC) complex that catalyzes chromatin loop formation. Here, we investigated how condensin is recruited to meiotic chromosomes in Saccharomyces cerevisiae. We show that double-strand break (DSB) formation, the initiating event of meiotic recombination, causes condensin redistribution from the nucleolus to DSB hotspots, pericentromeric regions and axis attachment sites. Hotspot association of condensin correlates weakly with break probability but does not depend on local DSB formation, whereas association with axis sites and pericentromeric regions depends on the Scc2-associated pool of cohesin, another SMC complex. Intriguingly, Scc2 distribution also changes in response to DSB formation. As condensin and Scc2-cohesin both catalyze chromatin loop extrusion, their redistribution upon DSB formation implies a profound change in chromatin loop dynamics that may help promote proper chromosome pairing and DNA repair.

2025-07-16 | GSE154722 | GEO

M18BP1 is a determinant of Condensin II activation

Project description:Condensin I and Condensin II promote drastic spatial compaction (condensation) of the genome upon mitotic entry. Condensin I binds chromatin only after dissolution of the nuclear envelope in prophase. Conversely, Condensin II is nuclear throughout the cell cycle and initiates chromosome condensation. Previous studies demonstrated that MCPH1 inhibits Condensin II to prevent chromosome condensation during interphase. Mechanisms that promote Condensin II activation in early mitosis likely exist but are currently unknown. Through genetic and proteomic approaches, we identify M18BP1, a protein previously associated with centromere identity, as a factor required for Condensin II localization to chromatin during mitosis. To activate and localize Condensin II, M18BP1 directly binds the CAP-G2 subunit. M18BP1 and MCPH1 compete for CAP-G2 binding, and CDK1 phosphorylation promotes replacement of MCPH1 with M18BP1 to activate Condensin II upon mitotic entry. Our results identify a fundamental and evolutionarily conserved mechanism of Condensin II activation

2025-11-03 | PXD051556 | Pride

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