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

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

PROVIDER: PRJNA1012303 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27955174_1.fastq.gz	Fastqsanger.gz
	SRR27955174_2.fastq.gz	Fastqsanger.gz
	SRR27955175_1.fastq.gz	Fastqsanger.gz
	SRR27955175_2.fastq.gz	Fastqsanger.gz
	SRR27955176_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: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 | GSE242222 | GEO

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

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

| PRJNA1012304 | ENA

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

2023-09-03 | GSE242223 | 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

| PRJNA485804 | ENA

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

Condensin I folds the C. elegans genome [Hi-C]

Project description:Structural Maintenance of chromosomes (SMC) complexes, cohesin and condensins, have been named after their roles during meiosis and mitosis. Recent data in mammalian cells and Drosophila have described the additional role of cohesin for genome folding into loops and domains during interphase. However, determinants of genome folding in holocentric species remain unclear. Using high resolution chromosome conformation capture, we show that overlapping large-scale nuclear localization and small-scale epigenomic states compartmentalize the C. elegans genome. By systematically and acutely inactivating each SMC complex, we observe that in contrast to other studied systems, cohesin creates small loops, while condensin I has a major role in genome folding: its inactivation causes genome-wide decompaction, chromosome mixing, loss of loops and TAD structures and reinforcement of fine-scale epigenomic compartments. Counter-intuitively, removal of condensin I and its X-specific variant condensin IDC from the X chromosomes led to the formation of a loop compartment coinciding with a subset of previously characterized loading sites for condensin IDC and bound by the X-targeting complex SDC. While transcriptional changes were limited for all autosomes upon cohesin and condensin II inactivation, removal of condensin I/IDC from the X chromosome led to transcriptional up-regulation of X-linked genes demonstrating that a sustained role for condensin IDC in gene regulation. Finally, while condensin I inactivation leads to reduced lifespan, we show that this reduction is due to X-specific gene upregulation rather than global genome decompaction.

2024-04-18 | GSE199721 | GEO

Molecular basis for condensin targeting to chromosomal loci [Hi-C]

Project description:Faithful chromosome segregation requires packaging of the genome on both global and local scales. Condensin plays a crucial role at pericentromeres to resist spindle forces and ensure the oriented attachment of kinetochores to microtubules at mitosis. Here we demonstrate that budding yeast condensin is recruited to pericentromeres through a direct interaction between its Ycg1 subunit and the pericentromeric adaptor protein, shugoshin (Sgo1). We identify a Short Linear Motif (SLiM), termed CR1, within the C-terminal region of Sgo1 which inserts into a conserved pocket on Ycg1. Disruption of this interface abolishes the Sgo1-condensin interaction, prevents condensin recruitment to pericentromeres and results in defective sister kinetochore biorientation in mitosis. Similar motifs to CR1 are found in known and potential condensin binding partners and the Ycg1 binding pocket is broadly conserved, including in mammalian CAP-G proteins. Overall, we uncover the molecular mechanism that targets condensin to define a specialized chromosomal domain.

2025-02-12 | GSE269442 | GEO

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