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Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76605 | GEO | 2017/08/17

SECONDARY ACCESSION(S): PRJNA308128

REPOSITORIES: GEO

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Massive reshaping of genome-nuclear lamina interactions during oncogene-induced senescence.

Project description: Not available

| S-EPMC5630027 | biostudies-literature

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (genome tiling)

Project description:Background. Cellular senescence is a mechanism that virtually irreversibly suppresses the proliferative capacity of cells in response to various stress signals. This includes the expression of activated oncogenes, which cause Oncogene-Induced Senescence (OIS). A body of evidence points to the involvement of chromatin reorganization, including the formation of senescence-associated heterochromatic foci (SAHF). The nuclear lamina (NL) is an important contributor to genome organization and has been involved in cellular senescence and organismal aging. It interacts with multiple regions of the genome called lamina-associated domains (LADs). Some LADs are cell type-specific, while others are conserved between cell types and are referred to as constitutive LADs. Here, we used DamID to investigate the changes in genome-NL interactions in a model of OIS triggered by the expression of the BRAFV600E oncogene. Results. We found that OIS cells lose most of their constitutive LADs (cLADS), suggesting the loss of a specific mechanism that targets cLADs to the NL. In addition, multiple genes relocated to the NL. Unexpectedly, they were not repressed, implying the abrogation of the repressive activity of the NL during OIS. Finally, OIS cells displayed an increased association of telomeres with the NL. Conclusions. Our study reveals that senescent cells acquire a new type of LAD organization and suggest the existence of as yet unknown mechanisms that tether cLADs to the NL and repress gene expression at the NL.

2017-08-17 | GSE76646 | GEO

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (DamID-seq)

2017-08-17 | GSE76594 | GEO

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (RNA-seq)

Project description:Cellular senescence is a mechanism that virtually irreversibly suppresses the proliferative capacity of cells in response to various stress signals. This includes the expression of activated oncogenes, which cause Oncogene-Induced Senescence (OIS). A body of evidence points to the involvement of chromatin reorganization, including the formation of senescence-associated heterochromatic foci (SAHF). The nuclear lamina (NL) is an important contributor to genome organization and has been involved in cellular senescence and organismal aging. It interacts with multiple regions of the genome called lamina-associated domains (LADs). Some LADs are cell type-specific, while others are conserved between cell types and are referred to as constitutive LADs. Here, we used DamID to investigate the changes in genome-NL interactions in a model of OIS triggered by the expression of the BRAFV600E oncogene. Results. We found that OIS cells lose most of their constitutive LADs (cLADS), suggesting the loss of a specific mechanism that targets cLADs to the NL. In addition, multiple genes relocated to the NL. Unexpectedly, they were not repressed, implying the abrogation of the repressive activity of the NL during OIS. Finally, OIS cells displayed an increased association of telomeres with the NL. Conclusions. Our study reveals that senescent cells acquire a new type of LAD organization and suggest the existence of as yet unknown mechanisms that tether cLADs to the NL and repress gene expression at the NL.

2017-08-17 | GSE75643 | GEO

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence

Project description:Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence

| PRJNA308128 | ENA

4D Genome Rewiring during Oncogene-Induced and Replicative Senescence.

Project description: Not available

| S-EPMC7208559 | biostudies-literature

Molecular maps of the reorganization of genome-nuclear lamina interactions during differentiation.

Project description: Not available

| S-EPMC5975946 | biostudies-literature

Local rewiring of genome-nuclear lamina interactions by transcription.

Project description: Not available

| S-EPMC7073462 | biostudies-literature

Genome-Nuclear Lamina Interactions Regulate Cardiac Stem Cell Lineage Restriction.

Project description: Not available

| S-EPMC5683101 | biostudies-literature

Evolutionary conservation of nuclear lamina-genome interactions

Project description:Regulation of gene expression is highly conserved between vertebrates, yet the genomic binding patterns of transcription factors are poorly conserved, suggesting that other mechanisms may contribute. The spatial organization of chromosomes in the nucleus is known to affect gene activity, but it is unclear to what extent this organization is conserved in evolution. Genome-wide maps of nuclear lamina (NL) interactions show that human and mouse chromosomes have highly similar folding patterns inside the nucleus. Breaks in synteny are often located at transition points between NL interacting and intra-nuclear regions. Data were compared against data from Peric-Hupkes, Meuleman et al. (Molecular Cell, 2010). LaminB1-chromatin interactions were assayed in human ESCs and human HT1080 cells. LaminA-chromatin interactions were assayed in human HT1080 cells. For the all samples there were 2 biological replicates, that were hybridized in a dye-swap design.

2012-10-10 | E-GEOD-22428 | biostudies-arrayexpress

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