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ATAC-seq in cultured renin lineage cells with the Lmna gene knockout.

ABSTRACT: ATAC-seq was performed to identify the effects in the knockout of the Lmna gene in renin lineage cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE167522 | GEO | 2021/05/26

REPOSITORIES: GEO

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ATAC-seq in cultured renin lineage cells with the Lmna gene knockout.

Project description:ATAC-seq in cultured renin lineage cells with the Lmna gene knockout.

| PRJNA704857 | 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

Gene expression profile in Lmna knockout mouse embryonic fibroblast

Project description:Alteration of gene expression profile due to Lmna knockout was studied in MEF. Total RNA obtained from Lmna +/+ MEF and Lmna -/- MEF were compared.

2012-06-18 | E-GEOD-38777 | biostudies-arrayexpress

ATAC-seq in myelinating oligodendrocytes from wt and Lmna knockout mice

Project description:We showed that the composition of the nuclear lamina changes with the differentiation state of oligodendrocyte lineage cells, with Lamin B highly expressed in progenitor cells and Lamin A highly expressed in mature oligodendrocytes. The genetic deletion of LMNA in mice results in the onset of a progressive motor phenotype in adult mice. We performed ATAC-Seq in myelinating Oligodendrocytes expressing the myelin marker NDRG1-EGFP ( Marechal et al., 2021) in the presence or absence of LMNA. The goal is to identify regions of chromatin accessibility that distinguish the LMNA KO mutant cells from the WT.

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Renin Regulatory Pathway Inhibition Epigenetically Silences *Ren1* (ATAC-Seq)

Project description:Background: Renin-expressing cells are myoendocrine cells crucial for survival which detect changes in blood pressure and release renin to maintain homeostasis. Renin is regulated through several pathways including cAMP, p300/CBP, and BET proteins including Brd4. Binding to the cAMP-responsive element in the renin enhancer region amplifies renin transcription and relies on each of these factors for an appropriate response. The specific regulatory changes that occur following inhibition of these pathways remains understudied. Therefore, we aimed to evaluate chromatin changes and gene signatures that occur following inhibition of renin regulatory factors. Methods: We treated As4.1 cells (a tumoral cell line that constitutively expresses renin) with three inhibitors (H89: PKA inhibition; JQ1: Brd4 inhibition; A-485: p300/CBP inhibition) that target required factors for renin transcriptional regulation. We then performed ATAC-seq, scRNA-seq, and ChIP-seq for H3K27ac and P300 binding on biological replicates of treated and control As4.1 cells. Results: Ren1 expression is significantly, but transiently, reduced following each inhibitory treatment. Further, PKA inhibition leads to corresponding losses in H3K27ac and p300 binding at the locus. A restricted set of nine genes with overlapping dynamically accessible regions, differential gene expression, and H3K27ac and p300 binding were identified with roles across three primary renin regulatory paradigms. Conclusions: The data shows that renin expression is regulated through a switch from an active to poised state of epigenetic control, a shift toward a less differentiated cellular identity via the loss of enhancer elements, and the disruption of cAMP, baroreceptor, and Notch mediated renin regulatory pathways.

2024-08-26 | GSE254940 | GEO

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

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

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Dysregulation of PDGFRB contributes to the pathogenesis of LMNA-related dilated cardiomyopathy [ATAC-seq]

Project description:Purpose: LMNA-DCM accounts for 5-10% of DCM cases and has an age-related penetrance whose onset typically appears between the ages of 30 and 40. However, the precise mechanisms linking the LMNA mutation to increased arrhythmogenicity are still unknown. Methods: We utilized human iPSC-CMs RNA-seq, ChIP-seq, and ATAC-seq technologies. Results: The electrophysiological studies of iPSC-CMs identify the LMNA mutation as a cause of increased arrhythmogenicity in mutant iPSC-CMs through abnormal calcium homeostasis. We find that the mutations in LMNA disrupt the global chromatin conformation, resulting in hyper-activation of the platelet-derived growth factor (PDGF) signaling pathway in LMNA-mutant iPSC-CMs. Inhibition of the PDGF signaling pathway can rescue the arrhythmic phenotype of mutant iPSC-CMs. Conclusions: These findings were corroborated in cardiac tissues from healthy and LMNA-DCM patients, thus confirming a novel mechanism of LMNA-DCM pathogenesis both in vitro and in vivo.

2019-07-05 | GSE118883 | GEO

scRNAseq libraries of pooled kidney samples from wild type (ZF1) versus CRISPR-targeted renin knockout (ZF2) zebrafish

Project description:Libraries were made to compare the transcriptome of renin lineage cells (RLCs) from wild-type versus ren knockout zebrafish kidneys. RLCs were FAC sorted from pooled kidneys of ren+/+ or ren-/- zebrafish, which carried ren:RFP and acta2:EGFP reporter genes, allowing the isolation of renin-expressing cells and smooth muscle cells.

2022-06-10 | E-MTAB-11079 | biostudies-arrayexpress

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