Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE190404 | GEO | 2023/06/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of myelinating oligodendrocytes in Lmna wt and knockout mice

Project description:We showed that the composition of the nucler 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 oligodendrocytes results in the onset of a progressive motor phenotype in adult mice. We performed RNA-Seq in myelinating oligodendrocytes expressing the reporter myelin marker NDRG1-EGFP ( Marechal et al., 2021) in the presence or absence of LMNA. The goal is to identify the transcriptome profile in mice LMNA ablated cells compared to the controls.

2023-06-21 | GSE222574 | GEO

Characterization of a newly-identified myelinating oligodendroglial population expressing NDRG1 in the adult mouse central nervous system

Project description:Oligodendrocytes are the main myelinating and remyelinating cells of the central nervous system. We identified N-myc downstream regulated gene family member 1 (NDRG1) as a specific mature marker of the oligodendroglial lineage, regulated by mTORC2 kinase activity. By generating a transgenic reporter murine line, we managed to precisely characterize the effect of cuprizone-induced treatment on myelinating cells. We also created a new and adult-specific whole genome transcriptomic profile of the oligodendroglial lineage, from proliferative OPC (using P60 PDGFRa::GFP sorted cells), to pre-myelinating OL (using P60 PLP::GFP sorted cells) and then mature OL (using P60 NDRG1-eGFP sorted cells). This new reporter murine line and its associated RNA-Sequencing dataset could help us better understand the specific biology of adult myelinating oligodendrocytes, compared to previously published developmental tools and databases.

2021-12-01 | GSE113614 | GEO

Induction of Myelinating Oligodendrocytes in Human Cortical Spheroids

Project description:Induction of Myelinating Oligodendrocytes in Human Cortical Spheroids

| PRJNA432547 | ENA

Induction of Myelinating Oligodendrocytes in Human Cortical Spheroids

Project description:Organoid technologies provide an accessible system in which to examine the generation, self-organization,and 3-dimensional cellular interactions during development of the human cerebral cortex. However, oligodendrocytes, the myelinating glia of the central nervous system and third major neural cell type, are conspicuously absent from current protocols. Here we reproducibly generate human oligodendrocytes and myelin in pluripotent stem cell-derived cortical spheroids. Transcriptional and immunohistochemical analysis of the spheroids demonstrates molecular features consistent with maturing human oligodendrocytes within 14 weeks of culture, including expression of MyRF, PLP1, and MBP proteins. Histological analysis by electron microscopy shows initial wrapping of human neuronal axons with myelin by 20 weeks and maturation to compact myelin by 30 weeks in culture. Treatment of spheroids with previously identified promyelinating drugs enhances the rate and extent of human oligodendrocyte generation and myelination. Furthermore, generation of spheroids from patients with a severe genetic myelin disorder, Pelizaeus-Merzbacher disease, demonstrates the ability to recapitulate human disease phenotypes, which were in turn improved with both pharmacologic and CRISPR-based approaches. Collectively, these 3-dimensional, multi-lineage cortical spheroids provide a versatile platform to observe and perturb the complex cellular interactions that occur during developmental myelination of the brain and offer new opportunities for disease modeling and therapeutic development in human tissue.

2018-07-30 | GSE110006 | GEO

Transcription profiling of rat perineuronal A2B5/OTMP+ oligodendrocytes

Project description:Oligodendrocytes are cells from the central nervous system that can be grouped into precursors, myelin-forming, and non-myelinating perineuronal. The function of perineuronal oligodendrocytes is unknown; it was suggested that they can ensheath denuded axons. We tested this hypothesis. Using cell-specific tags, microarray technology and bioinformatics tools to identify gene expression differences between these subpopulations allowed us to capture the genetic signature of perineuronal oligodendrocytes. Here we report that perineuronal oligodendrocytes are configured for a dual role. As perineuronal, they integrate a repertoire of transcripts designed to create a cell with its own physiological agenda. But they maintain a reservoir of untranslated transcripts encoding the major myelin proteins for â we speculate â a pathological eventuality. We posit that the signature molecules PDGFR-Î±Î², cytokine PDGF-CC, and the transcription factor Pea3 used â among others - to define the non-myelinating phenotype, may be critical for mounting a myelinating programme during demyelination. Harnessing this capability is of therapeutic value for diseases such as multiple sclerosis. This is the first molecular characterization of perineuronal oligodendrocytes. Experiment Overall Design: Flow Cytometry was used to isolate A2B5/OTMP+ oligodendrocytes from postnatal day 7 rat brain. 4 bioloical replicates were obtained. This data can be compared to the previously submitted oligodendrocyte expression data (GSE5940).

2008-06-18 | E-GEOD-11277 | biostudies-arrayexpress

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 profiles of livers from male LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed normal chow or high fat diet

Project description:To investigate the molecular basis for male-specific steatohepatitis in Lamin A/C-deficient livers, microarray gene expression analysis was performed on total liver RNA isolated from 26- to 39-week-old, male LMNA+/+, LMNA flx/+, and LMNA flx/flx; Alb-Cre+ C57BL/6 mice fed either normal chow (NC) or high fat diet plus carbohydrate-supplemented water (HFD). Lamins are nuclear intermediate filament proteins that comprise the major components of the nuclear lamina in metazoan cells. Mutations in LMNA, which encodes lamins A/C, cause diseases termed laminopathies, including lipodystrophy, cardiomyopathy, and premature aging. The lamin A/C mutation-associated Dunnigan familial partial lipodystrophy is typically accompanied by fatty liver disease. The role of lamins in the liver is unknown, and it is unclear whether laminopathy-associated liver disease is due to primary hepatocyte defects or systemic alterations. To address these questions, mice carrying a hepatocyte-specific deletion of Lmna (KO mice) were generated. KO hepatocytes manifested abnormal nuclear morphology, and KO mice developed spontaneous male-selective hepatosteatosis, with increased susceptibility to high fat diet-induced steatohepatitis and fibrosis. The molecular mechanism by which liver-specific Lamin A/C deficiency induces male-specific steatohepatitis is unknown. The microarray data presented here demonstrates that hepatic Lmna deficiency is associated with upregulated expression of fatty acid transporters, lipid biosynthetic enzymes, lipid-droplet associated proteins, and interferon-regulated genes and other pro-inflammatory mediators.

2017-01-16 | GSE93643 | 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

A2B5/OTMP+ rat perineuronal oligodendrocytes

Project description:Oligodendrocytes are cells from the central nervous system that can be grouped into precursors, myelin-forming, and non-myelinating perineuronal. The function of perineuronal oligodendrocytes is unknown; it was suggested that they can ensheath denuded axons. We tested this hypothesis. Using cell-specific tags, microarray technology and bioinformatics tools to identify gene expression differences between these subpopulations allowed us to capture the genetic signature of perineuronal oligodendrocytes. Here we report that perineuronal oligodendrocytes are configured for a dual role. As perineuronal, they integrate a repertoire of transcripts designed to create a cell with its own physiological agenda. But they maintain a reservoir of untranslated transcripts encoding the major myelin proteins for – we speculate – a pathological eventuality. We posit that the signature molecules PDGFR-αβ, cytokine PDGF-CC, and the transcription factor Pea3 used – among others - to define the non-myelinating phenotype, may be critical for mounting a myelinating programme during demyelination. Harnessing this capability is of therapeutic value for diseases such as multiple sclerosis. This is the first molecular characterization of perineuronal oligodendrocytes. Keywords: developmental

2008-06-01 | GSE11277 | GEO

Gene expression profiles of LMNA-V6 silencing or overexpression in HCT116 cells

Project description:Lamin A/C proteins, major components of the nuclear lamina, are encoded by the LMNA gene. These proteins have multiple cellular functions. LMNA has implications in cancer; however, its mechanisms of dysregulation in cancer cells are not yet fully understood. Among the LMNA transcript variants, we focused on a spliced variant 6 (termed LMNA-V6), which contains unique 3 exons upstream of exon 1 of LMNA. In this study, after LMNA-V6 levels were modulated by overexpression or silencing in colon cancer HCT116 cells, gene expression profiles were measured using microarray analysis.

2021-03-16 | GSE168912 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data