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Genome-wide maps of Lamin A-LADs binding affinity in control and LMNA R527C mutant MSCs

ABSTRACT: To determine if LMNA R527C mutation affect the arrangement and function of LADs, we performed Lamin A ChIP-seq in wild type and mutant MSCs. Reads of Lamin A ChIP-seq in LADs were decreased in mutant cells compared with wild type. These data suggested that the binding affinity of Lamin A to LADs was reduced after R527C mutation

ORGANISM(S): Homo sapiens

PROVIDER: GSE190196 | GEO | 2021/12/07

REPOSITORIES: GEO

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Genome-wide maps of LADs distribution in control and Dam-WT/Dam-R527C LMNA stabilized Hela cells

Project description:To determine if LMNA R527C mutation affect the arrangement and function of LADs, we performed Lamin A DamID-seq in wild type and mutant LMNA-stablized Hela cells. Reads of Lamin A ChIP-seq in LADs were decreased in mutant cells compared with wild type. These data suggested that the binding affinity of Lamin A to LADs was reduced after R527C mutation

2021-12-07 | GSE190197 | GEO

Genome-wide maps of chromatin openness in control and LMNA R527C mutant MSCs

Project description:We performed ATAC-seq to examine to chromatin of openness of coding genes in healthy control and LMNA R527C patient-derived MSCs. The reduction of LADs did not increase the accessibility of the promoters flanking coding genes. The genome wide analysis of ATAC-seq showed that openness of coding genes related chromatin was decreased in mutant MSCs.Thus, R527C mutant Lamin A led to dysfunction of LADs and dysregulation of gene transcription, probably, leading to slow down or arrest of cell proliferation and differentiation.

2021-12-07 | GSE190195 | GEO

Genome-wide maps of Lamin A-LADs binding affinity in control and LMNA R527C mutant MSCs

Project description:Genome-wide maps of Lamin A-LADs binding affinity in control and LMNA R527C mutant MSCs

| PRJNA786249 | ENA

ATAC-seq data from Lmna knock-out mouse embryonic fibroblasts (Lmna-/- MEFs) and wild type (Lmna+/+ MEFs)

Project description:Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.

2022-08-31 | GSE186677 | GEO

Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (expression)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. Total RNA obtained from ASCs and ASCs depleted of LMNA (LMNA-KD) and processed for microarray hybridization.

2013-07-14 | E-GEOD-42523 | biostudies-arrayexpress

Pre-patterning of differentiation-driven nuclear lamin A/C-associated chromatin domains by GlcNAcylated histone H2B

Project description:Dynamic interactions of nuclear lamins with chromatin through so-called lamin-associated domains (LADs) contribute to spatial arrangements of the genome. Here, we provide evidence for pre-patterning of differentiation-driven formation of lamin A/C LADs by domains of histone H2B modified by the nutrient sensor O-linked N-acetylglucosamine (H2BGlcNAc), which we term GADs. We demonstrate a two-step process of lamin A/C LAD formation during in vitro adipogenesis, involving (i) a spreading of lamin A/C-chromatin interactions during the transition from progenitor cell proliferation to cell cycle arrest, and (ii) a genome-scale redistribution these interactions through a process of LAD ‘exchange’ within hours of adipogenic induction. Chromatin state modeling reveals that lamin A/C LADs can be found both in active and repressive chromatin contexts which can be influenced by cell differentiation status. De novo formation of adipogenic lamin A/C LADs occurs non-randomly on GADs, consisting of megabase-size intergenic and repressive chromatin domains. Accordingly, while pre-differentiation lamin A/C LADs are gene-rich, post-differentiation LADs harbor repressive features reminiscent of lamin B1 LADs. Moreover, release of lamin A/C from genes directly involved in glycolysis concurs with their transcriptional upregulation after adipogenic induction, and with concordant downstream elevations in H2BGlcNAc levels and O-GlcNAc cycling. Our results unveil an epigenetic pre-patterning of adipogenic LADs by GADs, suggesting a coupling of developmentally regulated lamin A/C-genome interactions to a metabolically sensitive chromatin modification. Examination of LMNA and H2BGlcNAc binding in ASCs across differentiation

2015-09-04 | E-GEOD-63346 | biostudies-arrayexpress

Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (ChIPs and MeDips)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. ChIPs were done from cultured untreated and LMNA-downregulated adipose stem cell (ASC) chromatin. MeDIPs were done from LMNA-downregulated ASCs. ChIP and MeDIP DNA was hybridized onto the aforementioned HG-18 Nimbegen promoter arrays.

2013-07-14 | E-GEOD-42522 | biostudies-arrayexpress

High throughput sequencing of atypical progeria caused by LMNA R527C mutation

Project description:High throughput sequencing of atypical progeria caused by LMNA R527C mutation

| PRJNA786245 | ENA

ChIP-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

Project description:LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs) to the nuclear periphery. Mutations in LMNA cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, but the mechanisms are unknown. We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human fibroblasts throughout the cell cycle. pS22-Lamin A/C interacted with a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activator c-Jun. In progeria-patient fibroblasts, a subset of pS22-Lamin A/C-binding sites were lost whereas new pS22-Lamin A/C-binding sites emerged in normally quiescent loci. New pS22-Lamin A/C binding was accompanied by increased histone acetylation, increased c-Jun binding, and upregulation of nearby genes implicated in progeria pathophysiology. These results suggest that Lamin A/C regulates gene expression by enhancer binding. Disruption of the gene regulatory rather than LAD tethering function of Lamin A/C presents a novel mechanism for disorders caused by LMNA mutations.

2020-02-15 | GSE113291 | GEO

ATAC-seq reported in "Phosphorylated Lamin A/C in the nuclear interior binds active enhancers associated with abnormal transcription in progeria"

2020-02-15 | GSE113352 | GEO

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