Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA308323 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence
| PRJNA302675 | ENA
Project description:Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence
| PRJNA308128 | ENA
Project description:Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (DamID-seq)
| PRJNA308127 | ENA
Project description:We presented an adaptation of the TSA-seq antibody based method to map chromatin at the nuclear lamina from lower numbers of cells, which we term chromatin-based TSA-seq or cTSA-seq. We provide evidence that the method maps closed heterochromatin at or near the nuclear lamina that is in the B-compartment and show that it is useful down to 50,000 cells. We applied this emthod to the early G1 cell population to verify its utility and show that telomeric ends are indeed NL-proximal during this stage. We further provide evidence that the early G1 LADs profile is reminiscent of the profiles observed for oncogene-induced senescence.
2021-10-27 | GSE186503 | GEO
Project description:Lamina-associated domains (LADs) are megabase-sized portions of the genome anchored to the nuclear lamina (NL). Factors controlling the tethering of the genome to the NL have remained elusive. Here, we identified DNA Topoisomerase 2 beta (TOP2B) as a prominent regulator of genome-NL interactions. TOP2B depletion leads to the weakening of these interactions in LADs marked by H3K9me3 heterochromatin, and the repositioning of inter-LAD regions (iLADs) to the NL. TOP2B loss affects LAD interactions with Lamin B receptor (LBR) more prominently than with Lamins B1 and B2. LBR loss phenocopies the effects of TOP2B depletion, although the two proteins occupy different portions of the genome. Co-depletion of TOP2B and LBR causes partial LAD/iLADs inversion, mirroring changes typical of oncogene-induced senescence. We propose that a coordinated axis controlled by TOP2B in iLADs and LBR in LADs maintain proper partitioning of the genome between the NL and the nuclear interior.
2025-09-15 | GSE277501 | GEO
Project description:Lamina-associated domains (LADs) are megabase-sized portions of the genome anchored to the nuclear lamina (NL). Factors controlling the tethering of the genome to the NL have remained elusive. Here, we identified DNA Topoisomerase 2 beta (TOP2B) as a prominent regulator of genome-NL interactions. TOP2B depletion leads to the weakening of these interactions in LADs marked by H3K9me3 heterochromatin, and the repositioning of inter-LAD regions (iLADs) to the NL. TOP2B loss affects LAD interactions with Lamin B receptor (LBR) more prominently than with Lamins B1 and B2. LBR loss phenocopies the effects of TOP2B depletion, although the two proteins occupy different portions of the genome. Co-depletion of TOP2B and LBR causes partial LAD/iLADs inversion, mirroring changes typical of oncogene-induced senescence. We propose that a coordinated axis controlled by TOP2B in iLADs and LBR in LADs maintain proper partitioning of the genome between the NL and the nuclear interior.
2025-09-15 | GSE277502 | GEO
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
Project description:Lamina-associated domains (LADs) are megabase-sized genomic regions anchored to the nuclear lamina (NL). Factors controlling the interactions of the genome with the NL have largely remained elusive. Here, we identified DNA topoisomerase 2 beta (TOP2B) as a regulator of these interactions. TOP2B binds predominantly to inter-LAD (iLAD) chromatin and its depletion results in a partial loss of genomic partitioning between LADs and iLADs, suggesting that this enzyme might protect specific iLADs from interacting with the NL. TOP2B depletion affects LAD interactions with lamin B receptor (LBR) more than with lamins. LBR depletion phenocopies the effects of TOP2B depletion, despite the different positioning of the two proteins in the genome. This suggests a complementary mechanism for organising the genome at the NL. Indeed, co-depletion of TOP2B and LBR causes partial LAD/iLAD inversion, reflecting changes typical of oncogene-induced senescence. We propose that a coordinated axis controlled by TOP2B in iLADs and LBR in LADs maintains the partitioning of the genome between the NL and the nuclear interior.
2025-09-15 | GSE277500 | GEO
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
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 | GSE76594 | GEO