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Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE314558 | GEO | 2026/02/11

REPOSITORIES: GEO

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Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation. [RNA-Seq]

Project description:Lamin A/C is a crucial structural component of the nuclear lamina that influences chromatin organization and gene regulation. In this study, we demonstrate that lamin A/C is vital for maintaining higher-order genome organization and transcriptional programs that support EBV-driven B-cell activation. Loss of lamin A/C in a B-lymphoblastoid cell line caused significant three-dimensional reorganization of the genome, evidenced by the loss of long-range chromatin loops, an increase in short-range contacts, and redistribution of H3K9me2- marked heterochromatin. These structural disruptions were linked to widespread changes in gene expression affecting metabolic, signaling, and differentiation pathways. Mechanistically, lamin A/C influences the nuclear positioning and transcription of CTCF-bound loci by preventing their relocation to the periphery and their association with lamin B1. Blocking H3K9me2 deposition mimicked the transcriptional effects of lamin A/C depletion and revealed increased sensitivity to PI3K inhibitors. Overall, our results identify lamin A/C as a key organizer of genome structure and epigenetic regulation in EBV-infected B cells, uncovering a lamin-dependent pathway that connects nuclear architecture, metabolism, and viral disease processes.

2026-02-11 | GSE314537 | GEO

Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation. [Hi-C]

2026-02-11 | GSE314556 | GEO

Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation [ChiP-seq]

2026-02-11 | GSE314543 | GEO

Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.

Project description:Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.

| PRJNA1391501 | ENA

Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation. [RNA-Seq]

Project description:Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation. [RNA-Seq]

| PRJNA1391471 | ENA

Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation [ChiP-seq]

Project description:Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation [ChiP-seq]

| PRJNA1391483 | ENA

Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation. [Hi-C]

Project description:Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation. [Hi-C]

| PRJNA1391507 | ENA

Lamin B1 maintains the functional plasticity of nucleoli.

Project description:The dynamic ability of genomes to interact with discrete nuclear compartments appears to be essential for chromatin function. However, the extent to which structural nuclear proteins contribute to this level of organization is largely unresolved. To test the links between structure and function, we evaluated how nuclear lamins contribute to the organization of a major functional compartment, the nucleolus. HeLa cells with compromised expression of the genes encoding lamins were analyzed using high-resolution imaging and pull-down assays. When lamin B1 expression was depleted, inhibition of RNA synthesis correlated with complex structural changes within the nucleolar active centers until, eventually, the nucleoli were dispersed completely. With normal lamin expression, the nucleoli were highly plastic, with dramatic and freely reversible structural changes correlating with the demand for ribosome biogenesis. Preservation of the nucleolar compartment throughout these structural transitions is shown to be linked to lamin B1 expression, with the lamin B1 protein interacting with the major nucleolar protein nucleophosmin/B23.

| S-EPMC2722682 | biostudies-literature

CTCF regulates hepatitis B virus cccDNA chromatin topology

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

2024-01-18 | GSE249280 | GEO

Tcf1 is essential for initiation of oncogenic Notch1-driven chromatin topology in T-ALL.

Project description:NOTCH1 is a well-established lineage specifier for T cells and among the most frequently mutated genes throughout all subclasses of T cell acute lymphoblastic leukemia (T-ALL). How oncogenic NOTCH1 signaling launches a leukemia-prone chromatin landscape during T-ALL initiation is unknown. Here we demonstrate an essential role for the high-mobility-group transcription factor Tcf1 in orchestrating chromatin accessibility and topology, allowing aberrant Notch1 signaling to convey its oncogenic function. Although essential, Tcf1 is not sufficient to initiate leukemia. The formation of a leukemia-prone epigenetic landscape at the distal Notch1-regulated Myc enhancer, which is fundamental to this disease, is Tcf1-dependent and occurs within the earliest progenitor stage even before cells adopt a T lymphocyte or leukemic fate. Moreover, we discovered a unique evolutionarily conserved Tcf1-regulated enhancer element in the distal Myc-enhancer, which is important for the transition of preleukemic cells to full-blown disease.

| S-EPMC9710489 | biostudies-literature

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