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

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

PROVIDER: PRJNA485804 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10668707.fastq.gz	Fastqsanger.gz
	SRR10668708.fastq.gz	Fastqsanger.gz
	SRR10668709.fastq.gz	Fastqsanger.gz
	SRR10668710.fastq.gz	Fastqsanger.gz
	SRR10668711.fastq.gz	Fastqsanger.gz

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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:Senescence is induced by various stimuli such as oncogene expression and telomere shortening, referred to as oncogene-induced senescence (OIS) and replicative senescence (RS), respectively, and accompanied by global transcriptional alterations and 3D genome reorganization. Here, we demonstrate that the human condensin II complex participates in senescence via gene regulation and reorganization of euchromatic A and heterochromatic B compartments. Both OIS and RS are accompanied by A-to-B and B-to-A compartmental transitions, the latter of which occur more frequently and are undergone by 14% (430 Mb) of the human genome. Mechanistically, condensin is enriched in A compartments and implicated in B-to-A transitions. The full activation of senescence genes (SASP genes and p53 targets) requires condensin; its depletion impairs senescence markers. This study describes that condensin reinforces euchromatic A compartments and promotes B-to-A transitions, both of which are coupled to optimal expression of senescence genes, thereby allowing condensin to contribute to senescent processes.

| S-EPMC6908677 | biostudies-literature

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

| PRJNA1012297 | 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

Histone Demethylases KDM3A and KDM4C regulate mesenchymal stromal cell senescence and bone aging through condensin-mediated heterochromatin organization

Project description:Epigenomic changes and stem cell exhaustion are two hallmarks of aging. Accumulating evidence suggest that MSC senescence could perpetuate aging or age-related diseases. Here we report that two H3K9 demethylases KDM3A and KDM4C regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 in aging MSCs. Suppression of KDM3A or KDM4C leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 directly promotes heterochromatin reorganization and blunts DNA damage response. MSCs derived from kdm3a-/- mice exhibit compromised heterochromatin organization machinery and are more susceptible to genotoxic damage, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database for other human adult stem cells reveals inverse correlation of KDM3A and KDM4C with aging. Taken together, the present finding unveils a novel function of histone demethylases as a surveillance mechanism to restrain DNA damage accumulation via transcriptionally activating condensins during stem cell aging, which provides potential targets for the diagnosis and intervention of human aging and geriatric diseases.

2019-12-01 | GSE133098 | GEO

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]

| PRJNA1012303 | ENA

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

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (MBD-seq)

Project description:Primary cells enter replicative senescence after a limited number of cell divisions. This process is associated with reproducible changes in DNA methylation (DNAm) at specific sites in the genome. The mechanism that drives senescence-associated DNAm changes remains unknown and may arise through drift in DNAm or through regulated, senescence dependent modifications at specific sites in the genome. In this study, we analyzed the reorganization of nuclear architecture and DNA methylation during long-term culture of human fibroblasts and mesenchymal stromal cells (MSCs). [MethylCap-seq] Fibroblasts of two female donors (both 43 years old) were culture expanded and DNA was harvested of 10,000,000 cells at early passage (P3 or P5) and late passage (P30 and P33). DNA methylation changes were subsequently analyzed by MethylCap-Seq.

2015-03-26 | E-GEOD-59960 | biostudies-arrayexpress

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