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

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

PROVIDER: PRJNA1162536 | ENA |

REPOSITORIES: ENA

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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 (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

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

| PRJNA1162532 | ENA

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

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

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

| PRJNA1162535 | 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)

| PRJNA1162537 | ENA

DamID LaminB1 data in mouse MEFs, wild-type and POU2F1-/-. DamID LaminA data in mouse Neural Precursor Cells and Astrocytes.

Project description:DamID LaminB1 data were generated in POU2F1-/- MEFs to study the potential role of POU2F1/Oct1 in genome - nuclear lamina interactions. DamID LaminA data were generated in NPCs and Astrocytes to study similarities/differences between LaminA and LaminB1 binding. Comparison of MEF wt versus MEF POU2F1-/-. Comparison of LaminA (NPC & AC) with LaminB1 (NPC & AC data in GSE17051)

2012-10-10 | E-GEOD-36132 | biostudies-arrayexpress

The insulator protein SU(HW) modulates nuclear lamina interactions of the Drosophila genome: DamID

Project description:Specific interactions of the genome with the nuclear lamina (NL) are thought to assist chromosome folding inside the nucleus and to contribute to the regulation of gene expression. High-resolution mapping has recently identified hundreds of large, sharply defined lamina-associated domains (LADs) in the human genome, and suggested that the insulator protein CTCF may help to demarcate these domains. Here, we report the detailed structure of LADs in Drosophila cells, and investigate the putative roles of five insulator proteins in LAD organization. We found that of these five proteins, only SU(HW) binds preferentially at LAD borders and at specific positions inside LADs, while GAF, CTCF, BEAF-32 and DWG are mostly absent from these regions. By knockdown and overexpression studies we demonstrate that SU(HW) weakens LAD – NL interactions by a local antagonistic effect. Our results provide insights into the evolution of LAD organization and reveal a role for SU(HW) in the regulation of genome – NL interactions. DamID experiments for Lamin, CTCF, SU(HW), GAF, DWG, and BEAF-32, and for Lamin after overexpression and after knockdown of SU(HW), were performed in Drosophila cell cultures. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing. Every experiment was done in duplicate in the reverse dye orientation. The supplementary file 'GSE20311_DamID_norm_mean.txt' contains the mean log2(Dam-fusion/Dam-only) values of two replicates.

2011-01-24 | E-GEOD-20311 | biostudies-arrayexpress

LaminB1 DamID in undifferentiated mouse C2C12 myoblasts (ATCC, Lot 59501261) and differentiated C2C12 myotubes

Project description:Maps of genomic regions in proximity to the nuclear lamina were determined in undifferentiated C2C12 myoblasts (MBs) and 6 day differentiated C2C12 myotubes (MTs) using DamID with a Dam-Lamin B1-encoding lentivirus.

2016-06-17 | GSE80328 | GEO

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