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Global reorganisation of the nuclear landscape in senescent cells

ABSTRACT: Chandra, Ewels et al. mapped changes in genome organization in cellular senescence using HiC. Contrary to the believed increase in heterochromatin in senescence associated heterochromatic foci (SAHF) formation, they describe a loss of local interactions in heterochromatic regions. This is in agreement with changes observed in progeria cells.

PROVIDER: PRJEB8073 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR908499_1.fastq.gz	Fastqsanger.gz
	ERR908499_2.fastq.gz	Fastqsanger.gz
	ERR908500_1.fastq.gz	Fastqsanger.gz
	ERR908500_2.fastq.gz	Fastqsanger.gz
	ERR908501_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Global reorganisation of the nuclear landscape in senescent cells

Project description:Chandra, Ewels et al. mapped changes in genome organization in cellular senescence using HiC. Contrary to the believed increase in heterochromatin in senescence associated heterochromatic foci (SAHF) formation, they describe a loss of local interactions in heterochromatic regions. This is in agreement with changes observed in progeria cells.

| PRJEB8073 | ENA

Redistribution of the Lamin B1 genomic binding profile affects spatial rearrangement of heterochromatic domains and gene expression during senescence

Project description:Senescence is a stress responsive form of stable cell cycle exit. Senescent cells have a distinct gene expression profile, which is often accompanied by the spatial redistribution of heterochromatin into senescence-associated heterochromatic foci (SAHFs). Studying a key component of the nuclear lamina, lamin B1 (LMNB1), we report dynamic alterations in its genomic profile and their implications for SAHF formation and gene regulation during senescence. Genome-wide mapping reveals that LMNB1 is depleted during senescence, preferentially from the central regions of lamina-associated domains (LADs), which are enriched for H3K9me3. LMNB1 knockdown facilitates the spatial relocalization of perinuclear H3K9me3, thus promoting SAHF formation, which is inhibited by ectopic LMNB1 expression. Furthermore, despite the global reduction in LMNB1 protein levels, LMNB1 binding increases during senescence in a small subset of gene-rich regions where H3K27me3 also increases and gene expression becomes repressed. These results suggest that LMNB1 may contribute to senescence in at least two ways due to its uneven genomewide redistribution: firstly through the spatial re-organization of chromatin and, secondly, through gene repression. ChIP-seq for Lamin B1 in Growing and Ras Induced Senescence

2013-08-22 | E-GEOD-49341 | biostudies-arrayexpress

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

Nuclear RNA homeostasis promotes systems-level coordination of cell fate and senescence

Project description:Understanding cellular coordination remains a challenge despite knowledge of individual pathways. The RNA exosome, targeting a wide range of RNA substrates, is often downregulated in cellular senescence. Utilizing an auxin-inducible system, we observed that RNA exosome depletion in embryonic stem cells significantly affects the transcriptome and proteome, causing pluripotency loss and pre-senescence onset. Mechanistically, exosome depletion triggers acute nuclear RNA aggregation, disrupting nuclear RNA-protein equilibrium. This disturbance limits nuclear protein availability and hinders polymerase initiation and engagement, reducing gene transcription. Concurrently, it promptly disrupts nucleolar transcription, ribosomal processes, and nuclear exporting, resulting in translational shutdown. Prolonged exosome depletion induces nuclear structural changes resembling senescent cells, including aberrant chromatin compaction, chromocenter disassembly, and intensified heterochromatic foci. These effects suggest that dynamic turnover of nuclear RNA orchestrates crosstalk between essential processes to optimize cellular function. Disruptions in nuclear RNA homeostasis result in systemic functional decline, altering the cell state and promoting senescence.

2024-04-16 | GSE237465 | GEO

Lamin B1 overexpression alters chromatin organization and gene expression (Cut&Run-seq)

Project description:Overexpression of Lamin B1 leads to the redistribution of H3K9me3 heterochromatin away from the nuclear periphery and into heterochromatic DNA foci within the nucleoplasm. These changes in chromatin organization correlate with misregulated gene expression (mRNA-sequencing), but do not correlate with altered H3K9me3 deposition across the genome (Cut&Run).

2023-04-23 | GSE212108 | GEO

Lamin B1 overexpression alters chromatin organization and gene expression (mRNA-seq)

2023-04-23 | GSE212107 | GEO

Redistribution of the Lamin B1 genomic binding profile affects spatial rearrangement of heterochromatic domains and gene expression during senescence

2013-08-22 | GSE49341 | GEO

Exon array analysis in primary human fibroblasts

Project description:Exon usage analysis in in vitro cultured fibroblast cells. To assay the genome-wide splicing changes during cellular senescence, we performed splicing analysis on young and old normal fibroblasts, and in fibroblasts +/- tert (telomerase protein subunit Tert immortalized). We analyzed primary fibroblasts from 5 healthy subjects at various passages and from 2 Hutchinson-Gilford Progeria Syndrome (HGPS) patients using the Affymetrix Human Exon 1.0 ST platform. Two or three technical replicates were performed.

2011-06-17 | E-GEOD-28863 | biostudies-arrayexpress

Proteome analysis of serial-cultured human iPSC-derived MSC with lamin A/C mutation

Project description:Pathogenic mutations in lamin A/C (LMNA) lead to nuclear structural abnormalities, mesenchymal tissue damage, and laminopathies, which have numerous tissue-specific and progeria phenotypes. However, how LMNA mutations lead to accelerated mesenchymal-derived cell senescence remains unclear. Here, we established a replicative senescence model in vitro using induced pluripotent stem cell-derived mesenchymal stem cells (iMSCs) from patients with homozygous LMNA p.R527C mutation (LMNA R527C iMSCs). R527C iMSCs exhibited marked cell senescence and stemness potential attenuation, accompanied by immunophenotypic changes when expanded to passage 13 in vitro. Proteome analysis revealed that DNA replication, nuclear structure, and chromatin-related gene sets were the most significant changes in R527C iMSCs during replicative senescence, and pathways such as cell cycle, DNA replication, cell adhesion, and inflammation might play important roles in senescence.

2022-10-21 | PXD037639 |

Wnt5A promotes an adaptive, senescent-like stress response, while continuing to drive invasion in melanoma cells.

Project description:We have previously shown that Wnt5A drives invasion in melanoma. We have also shown that Wnt5A promotes resistance to therapy designed to target the BRAF(V600E) mutation in melanoma. Here, we show that melanomas characterized by high levels of Wnt5A respond to therapeutic stress by increasing p21 and expressing classical markers of senescence, including positivity for senescence-associated ?-galactosidase (SA-?-gal), senescence-associated heterochromatic foci (SAHF), H3K9Me chromatin marks, and PML bodies. We find that despite this, these cells retain their ability to migrate and invade. Further, despite the expression of classic markers of senescence such as SA-?-gal and SAHF, these Wnt5A-high cells are able to colonize the lungs in in vivo tail vein colony-forming assays. This clearly underscores the fact that these markers do not indicate true senescence in these cells, but instead an adaptive stress response that allows the cells to evade therapy and invade. Notably, silencing Wnt5A reduces expression of these markers and decreases invasiveness. The combined data point to Wnt5A as a master regulator of an adaptive stress response in melanoma, which may contribute to therapy resistance. To better understand the molecular mechanisms governing the response of highly invasive cells to IR as compared to that of poorly invasive cells, we performed microarray analysis of both poorly and highly invasive cells at early and late timepoints after irradiation. Cells were treated with y-irradiation, and RNA was taken at 1 hour, 24 hours and 5 days after irradiation. Microarray analysis was performed using Illumina Human HT-12 ver3 expression arrays, and each time point was compared to RNA from untreated cells.

2015-08-07 | E-GEOD-50004 | biostudies-arrayexpress

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