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Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (bTMP-seq)

ABSTRACT: Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (bTMP-seq)

PROVIDER: PRJNA1162535 | ENA |

REPOSITORIES: ENA

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Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor

Project description:Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor

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Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (pA-DamID)

Project description:Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (pA-DamID)

| PRJNA1162536 | ENA

Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (RNA-Seq)

Project description:Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (RNA-Seq)

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Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (bTMP-seq)

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

Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (RNA-Seq)

2025-09-15 | GSE277501 | GEO

Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (pA-DamID)

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

Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-09-15 | GSE277503 | GEO

Mapping the micro-proteome of the nuclear lamina and lamin associated domains

Project description:The nuclear lamina is a proteinaceous network of filaments that provide both structural and gene regulatory functions by tethering proteins and large domains of DNA, so-called lamin associated domains (LADs), to the periphery of the nucleus. LADs are a large fraction of the mammalian genome that are repressed, in part, by their association to the nuclear periphery. The genesis and maintenance of LADs is poorly understood as are the proteins that participate in these functions. In an effort to identify proteins that reside at the nuclear periphery and potentially interact with LADs, we have taken a two-pronged approach. First, we have undertaken an interactome analysis of the inner nuclear membrane bound LAP2β to further characterize the nuclear lamina proteome. To accomplish this, we have leveraged the BioID system, which previously has been successfully used to characterize the nuclear lamina proteome. Second, we have established a system to identify proteins that bind to LADs by developing a chromatin directed BioID system. We combined the BioID system with the m6A-tracer system which binds to LADs in live cells to identify LAD proximal and nuclear lamina proteins. In combining these datasets, we have further characterized the protein network at the nuclear lamina as well as identified putative LAD proximal proteins. Our analysis identifies many heterochromatin related proteins related to H3K9 methylation processes as well as many proteins related to cell cycle regulation identifying important proteins essential for LAD function.

2021-03-09 | PXD012943 | Pride

Stochastic genome-nuclear lamina interactions: Modulating roles of Lamin A and BAF

Project description:The nuclear lamina (NL) is a filamentous layer lining the inner-nuclear-membrane (INM) that aids in the organization of the genome in large domains of low transcriptional activity. Recently, it was shown that the single-cell genome-NL interactions are much more dynamic than previously anticipated, which challenges the concept of the NL as a safe guard for transcriptional repressed genes. Here we discuss the role of the NL in light of these new findings and introduce Lamin A and BAF as potential modulators of LAD positioning BAF-chromatin and Lamin B2-chromatin interactions were assayed in human HT1080 by DamID on Nimblegen microarrays, with two biological replicates each, that were hybridized in a dye-swap design.

2014-02-15 | E-GEOD-55066 | biostudies-arrayexpress

Lamina Associated Domains in MEFs depleted of specific lamin isotypes

Project description:Purpose: To compare the effects on Lamina Associated Domains (LADs) of shRNA treatment against lamin isotypes. Results: Using an optimized data analysis workflow (LADetector, available at https://github.com/thereddylab/LADetector), We found near identical sequences within the genome-wide maps indicating that ensemble methods are not effective for measuring random perturbations - perturbations that vary from cell to cell.

2020-07-07 | GSE153919 | GEO

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