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

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

PROVIDER: PRJNA786249 | ENA |

REPOSITORIES: ENA

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

Project description: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

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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.

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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

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Next Generation Sequencing Facilitates Quantitative Analysis of healthy donor- and LMNA R527C mutant patient-derived MSCs Transcriptomes

Project description:We reprogramed patient derived PBMCs into iPSCs, and differentiated the iPSCs into Mesenchymal stem cells. We performed whole genome wide RNA-seq of patient-derived MSCs and control MSCs. Up-regulated and down-regulated genes of LMNAR527C/R527C patient-derived MSCs were enriched and analyzed.

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

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

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Next Generation Sequencing Facilitates Quantitative Analysis of wild type and Lmna R527C mutant mice spleen Transcriptomes with or without 4Gy irradiation.

Project description:To induced the atypical progeria symptoms of LMNA R527C mutant mice, mutant and wild type mice were irradiated at 6 weeks of age with doses of 4 Gy. And to examine the pathologic change of mutant mice, mice were sacrificed at day -1and day 7 post-irradiation and spleen was harvested for RNAseq.

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Project description:Next Generation Sequencing Facilitates Quantitative Analysis of healthy donor- and LMNA R527C mutant patient-derived MSCs Transcriptomes

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Lamin A/C-dependent chromatin architecture safeguards naïve pluripotency to prevent aberrant cardiovascular cell fate and function [RNA-seq_ Lmna KD at CM]

Project description:Tight control of cell fate choices is crucial for normal development. Here we show that lamin A/C plays a key role in chromatin organization in embryonic stem cells (ESCs), which safeguards naïve pluripotency and ensures proper cell fate choices during cardiogenesis. We find major changes in chromatin compaction and localization of cardiac genes already in Lmna−/−ESCs resulting in precocious activation of a transcriptional program promoting cardiomyocyte versus endothelial cell fate, accompanied by premature cardiomyocyte differentiation, cell cycle withdrawal, and abnormal contractility. Gata4 is activated by lamin A/C loss and Gata4 silencing or haploinsufficiency rescues the aberrant cardiovascular cell fate choices induced by lamin A/C deficiency. Importantly, we observe divergent functions of lamin A/C in naïve pluripotent stem cells and cardiomyocytes, which has distinct contributions to the transcriptional alterations of patients with LMNA-associated cardiomyopathy. Thus, disruption of lamin A/C-dependent chromatin architecture in ESCs is a primary event in LMNA loss-of-function cardiomyopathy.

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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.

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

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