Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome wide analysis of RNA species present in SMN-containing RNPs

ABSTRACT: Several studies indicate that SMN-containing mRNP complexes could be involved in the axonal localization of a large number of mRNAs. We have used murine motor neuron-like NSC-34 cells and RNA Immuno-Precipitation experiments coupled to microarray analyses to perform a genome-wide analysis of RNA species present in mRNP complexes containing the full length SMN protein (flSMN). In situ hybridization and immuno-fluorescence experiments performed on several candidates indicate that these mRNAs colocalize with the SMN protein in neurites and axons of differentiated NSC-34 cells. Moreover, they localize in cell processes in a SMN-dependent manner. Thus, low SMN levels might result in localization deficiencies of mRNAs required for axonogenesis. RNA species coimmunoprecipitated with the SMN protein were used for hybridization of Affymetrix microarrays

ORGANISM(S): Mus musculus

SUBMITTER: johann Soret

PROVIDER: E-GEOD-40197 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Genome-wide identification of mRNAs associated with the protein SMN whose depletion decreases their axonal localization.

Rage Florence F Boulisfane Nawal N Rihan Khalil K Neel Henry H Gostan Thierry T Bertrand Edouard E Bordonné Rémy R Soret Johann J

RNA (New York, N.Y.) 20131023 12

Spinal muscular atrophy is a neuromuscular disease resulting from mutations in the SMN1 gene, which encodes the survival motor neuron (SMN) protein. SMN is part of a large complex that is essential for the biogenesis of spliceosomal small nuclear RNPs. SMN also colocalizes with mRNAs in granules that are actively transported in neuronal processes, supporting the hypothesis that SMN is involved in axonal trafficking of mRNPs. Here, we have performed a genome-wide analysis of RNAs present in compl ...[more]

PMID: 24152552

Similar Datasets

Genome wide analysis of RNA species present in SMN-containing RNPs

Project description:Several studies indicate that SMN-containing mRNP complexes could be involved in the axonal localization of a large number of mRNAs. We have used murine motor neuron-like NSC-34 cells and RNA Immuno-Precipitation experiments coupled to microarray analyses to perform a genome-wide analysis of RNA species present in mRNP complexes containing the full length SMN protein (flSMN). In situ hybridization and immuno-fluorescence experiments performed on several candidates indicate that these mRNAs colocalize with the SMN protein in neurites and axons of differentiated NSC-34 cells. Moreover, they localize in cell processes in a SMN-dependent manner. Thus, low SMN levels might result in localization deficiencies of mRNAs required for axonogenesis.

2013-11-29 | GSE40197 | GEO

ALS Associated Mutations in Matrin 3 Alter Protein-Protein Interactions and Impede mRNA Nuclear Export

Project description:Mutations in Matrin 3 have recently been linked to ALS, though the mechanism of disease in these patients is still unknown. To define the protein interactome of wild-type and ALS-linked MATR3 mutations, we performed immunoprecipitation followed by mass spectrometry experiments in NSC-34 cells expressing human wild-type or mutant Matrin 3. Gene ontology analysis identified a novel role for Matrin in mRNA transport centered around proteins in the TRanscription and EXport (TREX) complex, known to function in mRNA biogenesis and nuclear export. ALS-linked mutations in Matrin 3 led to its re-distribution within the nucleus, decreased co-localization with endogenous Matrin 3 and increased co-localization with TREX components. Expression of disease-causing Matrin 3 mutations led to nuclear mRNA export defects of both global mRNA and the mRNA of ALS linked proteins TDP-43 and FUS. Our findings demonstrate the first pathogenic mechanism attributable to MATR3 mutations and further link cellular transport defects to ALS.

2017-11-15 | PXD007710 | Pride

Interaction of 7SK with the Smn complex modulates snRNP production

Project description:Gene expression requires tight coordination of the molecular machineries that mediate transcription and splicing. While the interplay between transcription kinetics and spliceosome fidelity has been investigated before, less is known about mechanisms regulating the assembly of the spliceosomal machinery in response to transcription changes. Here we report an association of the Smn complex, which mediates spliceosomal snRNP biogenesis, with the 7SK complex involved in transcriptional regulation. We found that Smn interacts with the 7SK core components Larp7 and Mepce and specifically associates with 7SK subcomplexes containing hnRNP R. The association between Smn and 7SK complexes is enhanced upon transcriptional inhibition leading to reduced production of snRNPs. Taken together, our findings reveal a functional association of Smn and 7SK complexes that is governed by global changes in transcription. Thus, in addition to its canonical nuclear role in transcriptional regulation, 7SK has cytosolic functions in fine-tuning spliceosome production according to transcriptional demand.

2021-01-26 | PXD021360 | Pride

Multiple Molecular Pathways are influenced by Progranulin in a neuronal cell model

Project description:NSC-34 cells produced by fusing mouse embryonic spinal cord motor neuron with neuroblastoma cells expressing reduced level of PGRN (NSC-34/ShPGRN), NSC-34 cells overexpressing hPGRN(NSC-34-/hPGRN) or vector controls were compared in triplicate

2021-11-25 | MSV000088451 | MassIVE

Transcription profiling of mouse secondary neurospheres cultured from cells taken from mouse forebrains was compared between FoxO3+/+ (wildtype) and FoxO3-/- (null mutant) mice from the FVB/N background

Project description:In the nervous system, neural stem cells (NSC) are necessary for the generation of new neurons and for cognitive function. Here we show that FoxO3, a member of a transcription factor family known to extend lifespan in invertebrates, regulates the NSC pool. We find that adult FoxO3-/- mice have fewer NSC in vivo than wild type counterparts. NSC isolated from adult FoxO3-/- mice have decreased self-renewal and an impaired ability to generate different neural lineages. Identification of the FoxO3-dependent gene expression profile in NSC suggests that FoxO3 regulates the NSC pool by inducing a program of genes that preserves quiescence, prevents premature differentiation, and controls oxygen metabolism. The ability of FoxO3 to prevent the premature depletion of NSC might have important implications for counteracting brain aging in long-lived species. Experiment Overall Design: mRNA expression from secondary neurospheres cultured from cells taken from mouse forebrains was compared between FoxO3+/+ (wildtype) and FoxO3-/- (null mutant) mice from the FVB/N background.

2009-12-05 | E-GEOD-18326 | biostudies-arrayexpress

Compare gene expression profiles of mouse iNSC, WT-NSC, and MEF

Project description:The iNSC cells are two clones generated from the same MEF line. Therefore, we conducted one analysis that compared the two clonal lines and a separate analysis that compared iNSC vs. NSC, iNSC vs. MEF, and NSC vs. MEF. Both were single factor ANOVAs, the first compared two groups (the iNSC lines) and the second had three groups. For the second analysis, we then used linear contrasts to extract the information about differences between all pairs (e.g. iNSC vs. NSC). Looking at the iNSC lines, the correlations between samples from different clonal lines are as high as the correlations between samples from within a clonal line. Given this, we think that the analysis that combines all 6 of them to compare against the other cell types is appropriate. Array Platform: Affymetrix Mouse Gene 1.0 ST Samples: A total of 12 arrays array# filename genotype 1 01.iNSC1.1.CEL iNSC 2 02.iNSC1.2.CEL iNSC 3 03.iNSC1.3.CEL iNSC 4 04.iNSC2.1.CEL iNSC 5 05.iNSC2.2.CEL iNSC 6 06.iNSC2.3.CEL iNSC 7 07.WT.NSC.1.CEL NSC 8 08.WT.NSC.2.CEL NSC 9 09.WT.NSC.3.CEL NSC 10 10.WT.MEFs.1.CEL MEF 11 11.WT.MEFs.3.CEL MEF 12 12.WT.MEFs.5.CEL MEF

2012-06-06 | E-GEOD-37859 | biostudies-arrayexpress

Gene expression analysis of H9 hESC derived neuron stem cells (NSC) harboring pathogenic LRRK2 (G2019S) mutation

Project description:Genetic mutations on leucine-rich repeat kinase 2 (LRRK2) have been associated with an increased risk of Parkinson's disease. The Gly2019Ser (G2019S) mutation on LRRK2 gene is a relatively common cause of familial Parkinson's disease in Caucasian population. In this study, we generated H9 hESC harboring LRRK2 (G2019S) mutation by gene knockin. Wildtype and LRRK2 mutant hESC were differentiated into NSC using a chemically defined protocol. LRRK2 mutant NSC were treated with or without the LRRK2 kinase specific inhibitor (LRRK2-IN-1). Global gene expression analysis was performed to assess the overall similarity of gene expression profiles among three NSC groups (wildtype; LRRK2 mutant; LRRK2 mutant with inhibitor treatment).

2012-10-17 | E-GEOD-36321 | biostudies-arrayexpress

The histone H3.3K27M mutation in pediatric glioma reprograms H3K27 methylation and gene expression

Project description:Recent studies have identified a Lys 27-to-methionine (K27M) mutation at one allele of H3F3A, one of the two genes encoding histone H3 variant H3.3, in 60% of high-grade pediatric glioma cases. The median survival of this group of patients after diagnosis is ∼1 yr. Here we show that the levels of H3K27 di- and trimethylation (H3K27me2 and H3K27me3) are reduced globally in H3.3K27M patient samples due to the expression of the H3.3K27M mutant allele. Remarkably, we also observed that H3K27me3 and Ezh2 (the catalytic subunit of H3K27 methyltransferase) at chromatin are dramatically increased locally at hundreds of gene loci in H3.3K27M patient cells. Moreover, the gain of H3K27me3 and Ezh2 at gene promoters alters the expression of genes that are associated with various cancer pathways. These results indicate that H3.3K27M mutation reprograms epigenetic landscape and gene expression, which may drive tumorigenesis. We performed chromatin-immunoprecipitation of H3K27me3, H3K4me3, and EZH2 in SF7761 and NSC cell lines. And do RNA-seq in SF7761, SF8828 and NSC cell lines. SF7761 and SF8628 cell lines from patients harboring the histone H3.3 K27M mutation were obtained from Hashizume et al. (2012). NSCs (N7800-100) were purchased from Invitrogen and cultured and maintained in NSC medium (A10509-01, StemPro NSC SFM, Invitrogen).

2014-09-20 | E-GEOD-61586 | biostudies-arrayexpress

Microarray analysis of MCF7 cells treated with NSC 59687 (Oxyphenisatin Acetate)

Project description:NSC 59687 (oxyphenisatin acetate) is a novel anti-cancer agent with selectivity for breast and ovarian cell lines To elucidate the transcripts differentially regulated following treatment with Oxyphenisatin acetate (NSC 59687) MCF7 cells were treated with 10 microM NSC 59687 for 24 hours followed by RNA extraction, cDNA synthesis and microarray analysis using Affymetrix huU133 plus 2.0 arrays

2013-03-13 | E-GEOD-45046 | biostudies-arrayexpress

Tauroursodeoxycholic acid-induced neural stem cell proliferation

Project description:Tauroursodeoxycholic acid (TUDCA), an endogenous neuroprotective bile acid and a metabolic regulator, stimulates NSC proliferation and enhances adult NSC pool in vitro and in vivo. In this study, we dissected the mechanism triggered by this proliferation-inducing molecule, namely in mediating metabolic reprogramming. Liquid chromatography coupled with mass spectrometry based detection of differential proteomics revealed that TUDCA reduces the mitochondrial levels of the long-chain acyl-CoA dehydrogenase (LCAD), an enzyme crucial for β-oxidation of long-chain fatty acids (FA).

2021-09-09 | PXD017979 | Pride

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