Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene profiles regulated and targeted by PRC2 in oligodendrocyte lineage cells

ABSTRACT: The PRC2 complex creates a repressive mark histone-H3-Lys27-trimethylation. Although PRC2 is involved in various biological processes, its role in glial development remains ambiguous. We find PRC2 complex is required for oligodendrocyte (OL) differentiation and myelination, but not for OL precursor formation. Furthermore, most PRC2-null OL lineage cells (cKO) acquire astrocyte features. RNA profiles from RNAseq assay reveal that many transcription factors involved in oligodendrocyte and astrocyte development are regulated by PRC2. Moreover, PRC2-null OL lineage cells aberrantly induce Notch-NFIA and Wnt pathway genes. The chromatin immunoprecipitation-sequencing (ChIPseq) assay further reveals that PRC2 is recruited to many of Notch-NFIA and Wnt pathway genes. The datasets demonstrate the molecular program underlying the specific action of PRC2 and suggest PRC2 as a gatekeeper that determines the timing of OL lineage progression and myelination.

ORGANISM(S): Mus musculus

PROVIDER: GSE130628 | GEO | 2020/09/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GDE2-dependent activation of canonical Wnt signaling in neurons regulates

Project description:Neurons and oligodendrocytes communicate to regulate oligodendrocyte development and ensure appropriate axonal myelination. Here, we show that Glycerophosphodiester phosphodiesterase 2 (GDE2) encodes a neuronal pathway that promotes oligodendrocyte maturation through the release of soluble neuronally-derived factors. Mice lacking global or neuronal GDE2 expression have reduced mature oligodendrocytes and myelin proteins but retain normal numbers of oligodendrocyte precursor cells (OPCs). WT OPCs cultured in conditioned medium (CM) from Gde2 null (Gde2KO) neurons exhibit delayed maturation, recapitulating in vivo phenotypes. Gde2KO neurons show robust reduction in canonical Wnt signaling and genetic activation of Wnt signaling in Gde2KO neurons rescues in vivo and in vitro oligodendrocyte maturation. Phosphacan, a known stimulant of OL maturation, is reduced in CM from Gde2KOneurons but is restored when Wnt signaling is activated. These studies identify GDE2 control of Wnt signaling as a neuronal pathway that signals to oligodendroglia to promote oligodendrocyte maturation.

2021-09-09 | PXD018080 | Pride

Olig2 ablation in immature oligodendrocytes does not enhance CNS myelination and remyelination

Project description:The oligodendrocyte (OL) lineage gene Olig2 persistently expresses throughout oligodendroglial development and required for oligodendroglial specification and differentiation. Here, Together, by leveraging multiple immature OL-expressing Cre lines at different stages, we demonstrate that Olig2 is required for differentiation and myelination of immature OL and myelin repair and raise fundamental questions about the previously proposed role for Olig2 in opposing OL myelination, while highlighting the importance of using Cre-dependent reporter for lineage tracing in studying cell fate transition.

2022-11-23 | GSE194258 | GEO

The lncRNA genomic landscape of oligodendrocytes reveals myelination control by a lncOL1/Suz12 complex in the CNS [RNASeq_lncOL1]

Project description:Long noncoding RNAs (lncRNAs) are emerging as important regulators of cellular functions, but their roles in myelination in the CNS remain undefined. Through de novo transcriptome reconstruction at multiple stages, we establish dynamic expression profiles of lncRNAs during oligodendrocyte lineage progression and uncover a cohort of oligodendrocyte-enriched lncRNAs. Co-expression network analysis reveals a cohort of lncRNAs is linked to protein-coding genes associated with oligodendrocyte maturation. We identify a conserved chromatin-associated oligodendrocyte-restricted lncRNA, lncOL1. Overexpression of lncOL1 promotes oligodendrocyte differentiation in the developing brain, whereas genetic inactivation of lncOL1 causes defects in myelination and remyelination in the CNS. We further show that lncOL1 interacts with Suz12, a component of polycomb repressive complex 2, to promote oligodendrocyte differentiation in part through Suz12-mediated silencing of a differentiation inhibitory network that antagonizes OL maturation. Together, our findings demonstrate lncRNAs as a key layer of the genetic circuitry that controls CNS myelination and myelin repair.

2016-12-28 | GSE82210 | GEO

The lncRNA genomic landscape of oligodendrocytes reveals myelination control by a lncOL1/Suz12 complex in the CNS [RNASeq_DH]

2016-12-28 | GSE82209 | GEO

The lncRNA genomic landscape of oligodendrocytes reveals myelination control by a lncOL1/Suz12 complex in the CNS [ChIPSeq]

2016-12-28 | GSE82165 | GEO

Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [ATAC-seq]

Project description:Members of the Myt (myelin transcription factor) family have been implicated in neuronal development. However, their in vivo roles in OL lineage development have not been systematically investigated. Here, we identified Myt1 transcription factor as a crucial regulator of oligodendrocyte differentiation in the developing central nervous system. Conventional knockout of Myt1 causes a remarkable delay in the initiation of OL differentiation, without affecting the generation and proliferation of OPCs. Conversely, hyperactivation of Myt1 induces precocious OL differentiation both in vitro and in vivo. Using a combination of RNA-seq and ChIP-seq analyses, we identified Nkx2.2 as a key target of Myt1 to switch on the OL differentiation program. Mechanistically, specific binding of Myt1 in the Nkx2.2 gene loci inhibits the nucleosomal histone deacetylation via hindering the HDAC1 repressor complex integrity and reducing the deacetylation activity of HDAC1. Additionally, we demonstrated that Myt1 functions downstream of Notch signaling pathway in controlling the timing of OL differentiation. Collectively, our data demonstrate that Myt1 is a major regulator of OL differentiation and provide insight into the epigenetic regulatory mechanisms under OL development. Myt1 is, therefore, a promising therapeutic target for enhancing the OL differentiation and myelination/remyelination during development or after demyelination insults.

2024-10-01 | GSE253491 | GEO

Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [RNA-seq]

2024-10-01 | GSE253256 | GEO

Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [H3K9 ChIP-seq]

2024-10-01 | GSE253255 | GEO

Neural zinc finger protein Myt1 drives oligodendrocyte differentiation via repressing HDAC1-mediated histone deacetylation [MYT ChIP-seq]

2024-10-01 | GSE253254 | GEO

Sequentially Acting SOX Proteins Orchestrate Astrocyte and Oligodendrocyte Specific Gene Expression

Project description:SOX transcription factors have important roles during astrocyte and oligodendrocyte development, but how glial genes are specified and activated in a sub-lineage specific fashion remains unknown. To address this question, we have defined glial specific gene expression in the developing spinal cord using single-cell RNA-sequencing. Moreover, conducting ChIP-seq analyses we show that these glial gene sets are extensively preselected already in multipotent neural precursor cells through the prebinding by SOX3. In the subsequent lineage-restricted glial precursor cells, astrocyte genes become additionally targeted by SOX9 at DNA-regions strongly enriched for Nfi binding-motifs, whereas oligodendrocyte genes become prebound by SOX9 only, at sites that during oligodendrocyte maturation are targeted by SOX10. Interestingly, reporter gene assays and functional studies in the spinal cord revealed that SOX3 binding represses the synergistic activation of astrocyte genes by SOX9 and NFIA, whereas oligodendrocyte genes are activated in a combinatorial manner by SOX9 and SOX10. These genome-wide studies demonstrate how sequentially expressed SOX proteins act on lineage-specific regulatory DNA-elements to coordinate glial gene expression both in a temporal and sub-lineage specific fashion.

2018-08-02 | GSE117997 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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