Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Olig1/2 Coordinately Control Oligodendrocyte Versus Interneuron Fate Acquisition in Normal Brain and H3.3G34R/V-mutant Gliomas

ABSTRACT: Olig1/2 Coordinately Control Oligodendrocyte Versus Interneuron Fate Acquisition in Normal Brain and H3.3G34R/V-mutant Gliomas

PROVIDER: PRJNA1140536 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30004039_1.fastq.gz	Fastqsanger.gz
	SRR30004039_2.fastq.gz	Fastqsanger.gz
	SRR30004040_1.fastq.gz	Fastqsanger.gz
	SRR30004040_2.fastq.gz	Fastqsanger.gz
	SRR30004041_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Olig1/2 Coordinately Control Oligodendrocyte Versus Interneuron Fate Acquisition in Normal Brain and H3.3G34R/V-mutant Gliomas

Project description:The co-opting of the developmental gliogenesis program is a hallmark characteristic of glioblastoma (GBM). The bHLH transcription factors Olig1/2 are co-expressed in tri-potential intermediate progenitors (tri-IPCs) and GBM cells, yet their functions in these cells remain largely unknown. Here, we demonstrate that Olig1/2 coordinately promote the generation of oligodendrocytes while repressing the generation of olfactory bulb interneurons in tri-IPCs and GBM. Mechanistically, Olig1/2 directly bind to multiple enhancers, such as hs687, DSG (downstream from Gsx2) and a putative enhancer to regulate the expression of Gsx2, thereby regulating the fate determination process of tri-IPCs during gliogenesis. Furthermore, we provide compelling evidence that human histone H3.3G34R/V-mutation tumors, a subtype of pediatric high-grade gliomas, originate from cortical-derived tri-IPCs. Altogether, our findings suggest that the molecular mechanism of Olig1/2 in gliogenesis and gliomagenesis are conserved, which will deepen our understanding of the gaps between normal development and tumorigenesis.

2024-08-10 | GSE273171 | GEO

ID4 function antagonizes OLIG1 and OLIG2 to suppressive aggressive glioma

Project description:The basic helix-loop-helix proteins Olig1 and Olig2 are expressed in high grade, aggressive human glioblastoma multiformes (GBMs). Here we investigated genetic mechanisms regulating Olig1/2 function during gliomagenesis. Although Olig2 function is necessary for early-aggressive tumor formation in a genetically relevant model of classic GBMs with intact p53 function, late-onset gliomas do eventually form. Using an unbiased approach, we identified Id4, encoding a negative HLH protein, as a gene target potently repressed by Olig2 in glioma progenitors. Although Id4 is thought to antagonize proneural genes involved in differentiation, we report a paradoxical role for Id4 in glioma. Genetic deletion of Id4 converts Olig2-/- gliomas to the early-aggressive form, and conversely, overexpression of Id4 inhibits intact Olig2 and prevents even late-onset tumors. Olig1 overexpression is sufficient for gliomagenesis in an Id4-dependent manner. Together, these findings indicate that gliomagenic factors Olig1 and Olig2 are opposed by Id4 function, which acts as tumor suppressor in p53-intact gliomas.

2018-01-02 | GSE44151 | GEO

Transcription Factors Sp8 and Sp9 Coordinately Regulate Olfactory Bulb Interneuron Development

Project description:Transcription Factors Sp8 and Sp9 Coordinately Regulate Olfactory Bulb Interneuron Development

| PRJNA344717 | ENA

Expression analysis of neural stem cells isolated from Olig1-wt and Olig1-ko embryos

Project description:Olig1 is a bHLH transcription factor which is important for Oligodendrocyte development We used microarray profiling to assess which genes are differentially expressed in absence of Olig1 in neural stem cells. Neural stem cells were isolated from ganglionic eminences of E14.5 wild-type and Olig1-KO brains. The cells were cultured in serum-free neural stem cell media and RNA extracted.

2012-07-27 | E-GEOD-39706 | biostudies-arrayexpress

Expression analysis of neural stem cells isolated from Olig1-wt and Olig1-ko embryos

2012-07-28 | GSE39706 | GEO

Transcriptome changes in Olig1 over-expression retina ganglion cells (RGCs) by AAV-Olig1

Project description:To gain mechanistic insights into the effects of Olig1, we performed gene expression profiling analysis in RGCs. Transcriptome changes in Olig1 over-expression RGCs showed up-regulating genes related to axon projection development and regeneration-associated genes (RAGs), such as Stmn2, Gal, Gap43, and Sprr1a.

2022-12-30 | GSE221116 | GEO

Histone H3.3G34-mutant interneuron progenitors co-opt PDGFRA for gliomagenesis

Project description:Histone H3.3 glycine 34 to arginine/valine (H3.3G34R/V) mutations occur in deadly hemispheric high-grade gliomas. These tumors show exquisite regional and temporal specificity, suggesting a developmental context permissive to the effects of G34R/V mutations. Here we present the molecular landscape of G34R/V gliomas (n = 83) and show that ~50% bear activating mutations in PDGFRA, with strong selection pressure for PDGFRAMUT clones at recurrence. We show that G34R/V tumors arise in interneuron progenitors of the foetal ventral forebrain, expressing GSX2 and the DLX family of homeobox transcription factors, where terminal neuronal differentiation is impaired through aberrant G34R/V-mediated H3K27me3. Frequent co-occurrence of G34R/V & PDGFRAMUT is facilitated in this interneuron lineage-of-origin as PDGFRA forms an aberrant chromatin loop with the adjacent GSX2, hijacking its active chromatin conformation. At the single-cell level, G34R/V tumors entirely lack oligodendroglial transcriptional programs prominent in other glioma entities, and instead harbour dual neuronal and astroglial compartments. CRISPR-removal of H3.3G34R/V does not impact tumorigenicity suggesting this mutation becomes dispensable, while PDGFRAMUT are potently oncogenic regardless of G34 mutation. Collectively, our results suggest that G34R/V gliomas arise in foetal interneuron progenitors unable to terminally differentiate, enabling co-option of PDGFRA through inappropriate expression and activating mutations to promote gliogenesis and oncogenicity. Reliance on PDGFRA for oncogenesis may be of therapeutic opportunity in G34R/V glioma.

2020-11-30 | GSE146731 | GEO

Transcriptome changes in Olig1 over-expression retina ganglion cells (RGCs) by AAV-Olig1

Project description:Transcriptome changes in Olig1 over-expression retina ganglion cells (RGCs) by AAV-Olig1

| PRJNA912849 | ENA

New Olig1 null mice confirm a non-essential role for Olig1 in oligodendrocyte development.

Project description:BackgroundOlig1 and Olig2, encoding closely related basic helix-loop-helix transcription factors, were originally identified in screens for glial-specific genes. Olig1 and Olig2 are both expressed in restricted parts of the neuroepithelium of the embryonic spinal cord and telencephalon and subsequently in oligodendrocyte lineage cells throughout life. In the spinal cord, Olig2 plays a crucial role in the development of oligodendrocytes and motor neurons, and both cell types are lost from Olig2 null mutant mice. The role of Olig1 has been more cryptic. It was initially reported that Olig1 null mice (with a Cre-Pgk-Neo cassette at the Olig1 locus) have a mild developmental phenotype characterized by a slight delay in oligodendrocyte differentiation. However, a subsequent study of the same line following removal of Pgk-Neo (leaving Olig1-Cre) found severe disruption of oligodendrocyte production, myelination failure and early postnatal lethality. A plausible explanation was proposed, that the highly expressed Pgk-Neo cassette in the original line might have up-regulated the neighbouring Olig2 gene, compensating for loss of Olig1. However, this was not tested, so the importance of Olig1 for oligodendrocyte development has remained unclear.ResultsWe generated two independent lines of Olig1 null mice. Both lines had a mild phenotype featuring slightly delayed oligodendrocyte differentiation and maturation but no long-term effect. In addition, we found that Olig2 transcripts were not up-regulated in our Olig1 null mice.ConclusionsOur findings support the original conclusion that Olig1 plays a minor and non-essential role in oligodendrocyte development and have implications for the interpretation of studies based on Olig1 deficient mice (and perhaps Olig1-Cre mice) from different sources.

| S-EPMC3904929 | biostudies-literature

Comparative analysis of different cortical interneuron groups.

Project description:GABAergic interneuron in the cortex comprise a very heterogenous group. and it is critical to identify discrete interneuron types to understand how their contributions to behavior can be modulated by external and internal cues. However, molecular difinition of these interneuron cell groups has been difficult. Comparative analysis of different interneuron subtypes can provide us new candidate marker genes which could target more specific interneu?on cell group. Here we identify oxytocin responsive novel class of interneuron through our comparative analysis. We employed the bacTRAP strategy, which uses BAC transgenic mice expressing EGFP-tagged ribosomal protein L10a in specific cell populations, to affinity purify polysome-bound mRNAs from Nek7, Dlx1, Cort, Htr3a, Oxtr expressing cortical interneurons. We show that Oxtr expressing cells are a subtype of somatostatin positive interneurons. Three independent TRAP replicates were collected and total RNA from the immunoprecipitates or flow-through (input) whole cortex lysates were amplified and hybridized. Data were normalized with the GCRMA algorithm and replicates were averaged across conditions. We recommend filtering data to remove probe sets with normalized expression values less than 50 in at least one condition. Because the Nek7 BAC labels non-neuronal cells, we recommend to delete astrocytes and oligodendrocytes genes from the list using GSE13379 data.

2014-10-07 | E-GEOD-56996 | biostudies-arrayexpress

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