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Understanding the transcriptional consequences of the Progeria LmnaG609G mutation within the immune compartment of the lung using single cell RNA sequencing.

ABSTRACT: Understanding the transcriptional consequences of the Progeria LmnaG609G mutation within the immune compartment of the lung using single cell RNA sequencing.

PROVIDER: PRJNA759785 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15697800_1.fastq.gz	Fastqsanger.gz
	SRR15697800_2.fastq.gz	Fastqsanger.gz
	SRR15697801_1.fastq.gz	Fastqsanger.gz
	SRR15697801_2.fastq.gz	Fastqsanger.gz
	SRR15697802_1.fastq.gz	Fastqsanger.gz

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Understanding the transcriptional consequences of the Progeria LmnaG609G mutation within the immune compartment of the lung using single cell RNA sequencing.

Project description:To understand the transcriptional consequences of Progeria LmnaG609G mutation within the immune compartment of the lung we conducted single cell RNA sequencing on sorted immune cells from WT vs. LmnaG609G/G609G mice (in duplicate, 2 mice per group).

2024-08-01 | GSE183249 | GEO

Understanding the transcriptional consequences of Lamin A deficiency within the immune compartment of the lung using single cell RNA sequencing.

Project description:To understand the transcriptional consequences of Lamin A deficiency within the immune compartment of the lung we conducted single cell RNA sequencing on sorted immune cells from WT vs. Lmna-flox/flox Vav1-cre-/- mice (in duplicate, 2 mice per group).

2023-07-24 | GSE146080 | GEO

Understanding the transcriptional consequences of Lamin A deficiency within the immune compartment of the lung using single cell RNA sequencing.

Project description:Understanding the transcriptional consequences of Lamin A deficiency within the immune compartment of the lung using single cell RNA sequencing.

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CscoreTool-M infers 3D sub-compartment probabilities within cell population

Project description:Motivation: Computational inference of genome organization based on Hi-C sequencing has greatly aided the understanding of chromatin and nuclear organization in three dimensions (3D). However, existing computational methods fail to address the cell population heterogeneity. Here we describe a probabilistic modeling-based method called CscoreTool-M that infers multiple 3D genome sub-compartments from Hi-C data. Results: The compartment scores inferred using CscoreTool-M represents the probability of a genomic region locating in a specific sub-compartment. Compared to published methods, CscoreTool-M is more accurate in inferring sub-compartments corresponding to both active and repressed chromatin. The compartment scores calculated by CscoreTool-M also help to quantify the levels of heterogeneity in sub-compartment localization within cell populations. By comparing proliferating cells and terminally differentiated non-proliferating cells, we show that the proliferating cells have higher genome organization heterogeneity, which is likely caused by cells at different cell-cycle stages. By analyzing 10 sub-compartments, we found a sub-compartment containing chromatin potentially related to the early-G1 chromatin regions proximal to the nuclear lamina in HCT116 cells, suggesting the method can deconvolve cell cycle stage-specific genome organization among asynchronously dividing cells. Finally, we show that CscoreTool-M can identify sub-compartments that contain genes enriched in housekeeping or cell-type-specific functions. Availability: https://github.com/scoutzxb/CscoreTool-M

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Single-Dose CRISPR/Cas9 Therapy Extends Lifespan of Mice with Hutchinson-Gilford Progeria Syndrome

Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare lethal genetic disorder characterized with symptoms reminiscent of accelerated aging. The major underlying genetic cause is a substitution mutation in the gene coding for lamin A, causing the production of a toxic isoform called progerin. Here we show the RNA sequencing analyses performed on primary mouse fibroblasts of different genotypes (in terms of Progeria; Cas9 background) treated with Cas9 guide RNAs targeting Lmna/Progerin. The mouse genetic background in (1) Pro/Pro;Cas9/+: homozygous for Progeria and heterozygous for transgenic Cas9 The mouse genetic background in (2) Pro/+; +/+: heterozygous for Progeria and no transgenic Cas9 (wild type) The mouse genetic background in (3) +/+;Cas9/+: no Progeria (wild type) and heterozygous for transgenic Cas9

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Project description:This SuperSeries is composed of the following subset Series: GSE41751: Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (expression) GSE41757: Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (ChIP-seq) GSE41763: Correlated alterations in genome organization, histone methylation, and DNA-lamina interactions in Hutchinson-Gilford progeria syndrome (Hi-C) Refer to individual Series

2012-10-30 | E-GEOD-41764 | biostudies-arrayexpress

Recapitulation of human premature aging by using iPSCs from Hutchinson-Gilford progeria syndrome

Project description:Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal human premature aging disease1-5, characterized by premature atherosclerosis and degeneration of vascular smooth muscle cells (SMCs)6-8. HGPS is caused by a single-point mutation in the LMNA gene, resulting in the generation of progerin, a truncated mutant of lamin A. Accumulation of progerin leads to various aging-associated nuclear defects including disorganization of nuclear lamina and loss of heterochromatin9-12. Here, we report the generation of induced pluripotent stem cells (iPSCs) from fibroblasts obtained from patients with HGPS. HGPS-iPSCs show absence of progerin, and more importantly, lack the nuclear envelope and epigenetic alterations normally associated with premature aging. Upon differentiation of HGPS-iPSCs, progerin and its associated aging consequences are restored. In particular, directed differentiation of HGPS-iPSCs to SMCs leads to the appearance of premature senescent SMC phenotypes associated with vascular aging. Additionally, our studies identify DNA-dependent protein kinase catalytic subunit (DNAPKcs) as a component of the progerin-containing protein complex. The absence of nuclear DNAPKcs correlates with premature as well as physiological aging. Since progerin also accumulates during physiological aging6,12,13, our results provide an in vitro iPSC-based model with an acceleration progerin accumulation to study the pathogenesis of human premature and physiological vascular aging. Microarray gene expression profiling was done to: (1) Compare differences between WT fibroblasts and fibroblasts from patients suffering of the Hutchinson-Gilford progeria syndrome (2) Check that iPSC originating from WT and patients are in fact similar to ESC

2011-03-14 | E-GEOD-24487 | 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

Endothelial-to-mesenchymal transition contributes to accelerated atherosclerosis in Hutchinson–Gilford progeria syndrome

Project description:The main goal of this study was to gain insight into the mechanisms underlying phenotypic changes in endothelial cells during atherosclerosis associated with Hutchinson-Gilford progeria syndrome, a premature aging syndrome. To this end, we performed an RNAseq experiment with aortic intima samples from atheroprone mice with ubiquitous and VSMC-specific progeria expression and their corresponding controls.

2024-06-05 | GSE269166 | GEO

In vitro methylation studies in human fibroblasts from progeria cases

Project description:An Infinium microarray platform (GPL23976, Illumina Infinium HumanMethylation850 BeadChip) was used to generate DNA methylation data from fibroblasts from human progeria cases. Treatment: Antisense oligonucleotide for Line 1 elements.

2022-04-13 | GSE200152 | GEO

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