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Transcriptome of early postnatal brain development of eIF2B-R132H/R132H mutant mice relative to wild-types.

ABSTRACT: Genome-wide mRNA expression in brains of wild-type and eIF2B-R132H/R132H mutant mice (Geva et al., BRAIN 133 (8), 2010) profiled at postnatal (P) days 1, 18 and 21 to reflect the early proliferative stage prior to white matter establishment (P1) and the peak of oligodendrocye differentiation and myelin synthesis (P18 and P21).

ORGANISM(S): Mus musculus

PROVIDER: GSE32201 | GEO | 2011/11/14

SECONDARY ACCESSION(S): PRJNA147387

REPOSITORIES: GEO

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Transcriptome of early postnatal brain development of eIF2B-R132H/R132H mutant mice relative to wild-types.

Project description:Genome-wide mRNA expression in brains of wild-type and eIF2B-R132H/R132H mutant mice (Geva et al., BRAIN 133 (8), 2010) profiled at postnatal (P) days 1, 18 and 21 to reflect the early proliferative stage prior to white matter establishment (P1) and the peak of oligodendrocye differentiation and myelin synthesis (P18 and P21). 3 biological replicates (whole brain without the cerebellum) from each wild-type and eIF2B-R132H/R132H mutant mice at 3 postnatal (P) days 1, 18 and 21 were used for RNA extraction and hybridization on Affymetrix microarrays.

2011-11-14 | E-GEOD-32201 | biostudies-arrayexpress

eIF2B links translational control to mitochondrial oxidative phosphorylation in Vanishing White Matter disease

Project description:Eukaryotic translation initiation factor 2B is a master regulator of protein synthesis under normal and stress conditions. Mutations in any of the five genes encoding its subunits lead to Vanishing White Matter (VWM) disease, a recessive genetic deadly illness caused by progressive loss of white matter in the brain. Although fibroblasts are not involved in the disease, we used mouse embryo fibroblasts (MEFs) isolated from Eif2b5R132H/R132H mice to demonstrate their compromised mitochondrial translation, unbalanced stoichiometry of proteins involved in oxidative phosphorylation, decreased basal and maximal oxygen consumption rate, and increased mitochondrial abundance reflecting adaptation to meet energy requirements. The involvement of eIF2B in mitochondrial function and abundance was validated in primary astrocytes isolated from Eif2b5R132H/R132H mice brains. We found that oxidative respiration deficiency is more robust in astrocytes and does not reach normal cellular levels even following 2-fols increase in mitochondrial content. The consequent increase in basal and maximal glycolysis in mutant astrocytes demonstrates their enhanced sensitivity to the impaired oxidative phosphorylation, illuminating the importance of mitochondrial function in VWM pathology. The data demonstrates the critical role of eIF2B in tight coordination of expression from nuclear and mitochondrial genomes. Further dissection of the signalling network associated with eIF2B function will help generating therapeutic strategies for VWM disease and possibly other neurodegenerative disorders.

2017-07-11 | PXD005854 | Pride

DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation

Project description:This SuperSeries is composed of the following subset Series: GSE31126: DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation [Affymetrix] GSE31133: DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation [Illumina] Refer to individual Series

2012-08-12 | E-GEOD-31134 | biostudies-arrayexpress

Differential gene expression in IDH1-R132H Tumor Neurospheres generated from a mouse model of Low Grade Glioma

Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylatyed phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt tumor neurospheres.

2019-03-18 | GSE94974 | GEO

Gene expression analysis of IDH1 wild type and IDH1 R132H mutated U87 cells

Project description:U87 cells were transduced with IDH1 WT or IDH1 R132H and stable clones were selected.

2018-07-12 | GSE101291 | GEO

Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

Project description:To investigate whether IDH1 mutation influence the effects of oncolytic virus VSVΔ51, we transduced doxycycline-inducible IDH1-R132H lentiviruses into LN-229 to establish the LN-229-TRE-R132H cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of LN-229-TRE-R132H cells infected with or without VSVΔ51 in the presence or absence of IDH1 mutation induced by doxycycline.

2023-09-19 | GSE208634 | GEO

Idh1-R132H mutation increases murine hematopoietic progenitors and alters epigenetics.

Project description:Mutations in the IDH1 and IDH2 genes encoding isocitrate dehydrogenases are frequent in human glioblastomas1 and cytogenetically normal acute myeloid leukemias (AML)2. These alterations are gain-of-function mutations in that they drive the synthesis of the M-bM-^@M-^\oncometaboliteM-bM-^@M-^] R-2-hydroxyglutarate (2HG)3. It remains unclear how IDH1 and IDH2 mutations modify myeloid cell development and promote leukemogenesis. Here we report the characterization of conditional knock-in mice in which the most common IDH1 mutation, Idh1-R132H, is inserted into the endogenous murine Idh1 locus and is expressed in cells of the hematopoietic (Vav-KI) or more specifically in cells of the myeloid (LysM-KI) lineage. These mutants show increased numbers of early hematopoietic progenitors and develop splenomegaly and anemia with extramedullary hematopoiesis, suggesting a dysfunctional bone marrow niche. Furthermore, LysM-KI cells exhibit both hypermethylated histones and changes to DNA methylation similar to those observed in human IDH1/2-mutant AML. Thus, our study is the first to describe the generation of conditional Idh1-R132H-KI mice. Furthermore, our study is also the first report showing the induction of a leukemic DNA methylation signature in a modeled system and sheds light on the mechanistic links between IDH1 mutation and human AML. DNA methylation profiling in LSK cells from IDH1-R132H knock-in mice vs. control mice

2012-07-22 | E-GEOD-38687 | biostudies-arrayexpress

Differential gene expression in IDH1-R132H Low Grade Glioma animal brain tumors brain in response to 10 Gy of radiation

Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with loss of function mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylatyed phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt LLG animal brain tumors in reponse to radiation

2019-03-18 | GSE94975 | GEO

Differential gene expression in IDH1-R132H low grade glioma animal brain tumors brain in response to 20 Gy of radiation

Project description:IDH1-R132H is expressed in Low Grade Glioma (LGG) in combination with loss of function mutation in ATRX and TP53 genes. IDH1-R132H results in gain of function with production of 2-hydroxygluatrate, that in turn generates a hypermethylated phenotype in DNA and histone with consequences in epigenetic regulation of gene expression. Here we will compare the gene expression profile between IDH1-R132H and IDH1 Wt LLG moribund animal brain tumors and identify key genes responsible for the phenotype of this subtype of glioma.

2018-02-10 | GSE94902 | GEO

Developmental maturation but no sex-dependent divergence of the murine CNS myelin proteome

Project description:To assess whether the CNS myelin proteome varies within the same species, we used quantitative mass spectrometry to compare myelin purified from mouse brains at three developmental timepoints (P18, P75, 6 months), brains of male and female mice, and four CNS regions (cortex, corpus callosum, optic nerve, spinal cord). We utilized a data-independent acquisition (DIA) workflow with alternating low and elevated energy (MSE) and an ion mobility-enhanced version thereof (referred to as UDMSE) to achieve both, a correct quantification of exceptionally abundant myelin proteins and a comprehensive coverage of the myelin proteome. Label-free protein quantification revealed that the myelin protein composition matures between P18 and P75, and remains largely similar up to 6 months. Proteins with decreasing abundance included cytoskeleton-associated proteins (regulating sheath growth and wrapping), whereas proteins with increasing abundance included all subunits of the septin filament (stabilizing mature myelin), and potentially protective proteins. Among the latter was quinoid dihydropteridine reductase (QDPR), which emerges as a highly specific marker for mature oligodendrocytes and myelin. Conversely, female and male mice display essentially similar myelin proteomes and the myelin-enriched fractions from the four CNS regions mainly differ by the abundance of HCN2-channels in spinal cord myelin as a requirement for particularly long sheaths, apart from the extent of contaminating mitochondrial and synaptic proteins.

2024-08-27 | PXD053062 | Pride

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