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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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			Action	DRS
	SRR17133695_1.fastq.gz	Fastqsanger.gz
	SRR17133695_2.fastq.gz	Fastqsanger.gz
	SRR17133696_1.fastq.gz	Fastqsanger.gz
	SRR17133696_2.fastq.gz	Fastqsanger.gz
	SRR17133697_1.fastq.gz	Fastqsanger.gz

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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

2021-12-07 | GSE190196 | 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 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

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.

2021-12-07 | GSE190198 | GEO

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

| PRJNA786250 | ENA

Lamin C supplementation as therapeutic target for treatment of Lmna Dilated Cardiomyopathy (DCM) and risk of Lamin A toxicity

Project description:Dilated cardiomyopathy (DCM) is a severe, non-ischemic heart disease, which ultimately results in heart failure (HF). Pathological genetic variants in LMNA cause DCM, which currently lacks specific treatment. Perturbing candidates related to dysregulated pathways have shown to ameliorate LMNA DCM, but their long-term efficacy as potential therapeutic targets is unknown. Here, we evaluated 14 potential candidates including Lmna gene products, key signaling pathways, calcium handling, proliferation regulators and Lamin interacting proteins, in a cardiac-specific Lmna DCM model. The candidates with improved cardiac function were further assessed through survival analysis. After comparing cardiac function, marker gene expression, Tgfβ signaling pathway activation, fibrosis, inflammation, proliferation, and DNA damage, we uncovered that restored cardiac function significantly correlated with suppression of HF/fibrosis marker expression and cardiac fibrosis in Lmna DCM. Interestingly, Lamin C or Sun1 shRNA administration achieved consistent, prolonged survival which highly correlated with reduced heart inflammation and DNA damage. In addition to Sun1 shRNA, perturbing the interaction between the nucleoskeleton and cytoskeleton via the KASH domain of Nesprin1 also effectively suppressed Lmna DCM. In contrast, Lamin A supplementation did not rescue long term survival and may impart a detrimental cardiotoxicity risk. Furthermore, transcriptome profiling was used to compare the differences between Lamin A and Lamin C treatment. Mechanistically, we identified that this lapse was attributed to a dose-dependent toxicity of Lamin A, which was independent of its maturation. This study highlights the potential for advancing Lamin C and Sun1 as therapeutic targets for the treatment of LMNA DCM.

2024-08-11 | GSE240745 | GEO

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

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

| PRJNA786247 | ENA

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.

2021-12-07 | GSE190199 | GEO

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

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.

2022-10-11 | GSE164065 | GEO

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