Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hippocampal expression data from WT, KO, R270X, and G273X mice at 4 and 9 weeks

ABSTRACT: Mecp2 loss-of-function has been associated with altered gene expression in many tissues. We characterized gene expression changes within the hippocampi of 3 different Mecp2 loss-of-function mouse models. These studies were used to identify transcriptional differences between these mutants when the mice are largely asymptomatic (4 weeks of age) or have developed overt phenotypes (9 weeks).

ORGANISM(S): Mus musculus

PROVIDER: GSE42987 | GEO | 2013/03/22

SECONDARY ACCESSION(S): PRJNA184020

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Hippocampal expression data from WT, KO, R270X, and G273X mice at 4 and 9 weeks

Project description:Mecp2 loss-of-function has been associated with altered gene expression in many tissues. We characterized gene expression changes within the hippocampi of 3 different Mecp2 loss-of-function mouse models. These studies were used to identify transcriptional differences between these mutants when the mice are largely asymptomatic (4 weeks of age) or have developed overt phenotypes (9 weeks). Hippocampal expression data from WT (Mecp2+/y), KO (Mecp2-/y), R270X (Mecp2-/y,R270XTg), and G273X (Mecp2-/y,G273XTg) mice at 4 and 9 weeks At total of 32 microarrays were performed: 4 animals of each genotype at both 4 weeks and 9 weeks of age.

2013-03-22 | E-GEOD-42987 | biostudies-arrayexpress

Transcriptome analysis of a MECP2 conditional KO mouse model

Project description:Rett syndrome is a severe neurodevelopmental condition that rsults primarily from mutations in the MECP2 gene. MECP2 is known to function as both a transcriptional activator and transcriptional repressor. However, it remains unclear how transcriptional dysregulation resulting from MECP2 mutations lead to the Rett syndrome phenotype. Multiple mouse models have been generated to investigate the function of MECP2 in vivo. Remarkably, despite the neurodevelopmental phenotype characteristic of Rett syndrome, temporal conditional MECP2 knock-out mouse models with MECP2 deletion induced postnatally recapitulate the Rett-syndrome-like phenotype in mouse. Here we investigated gene expression changes in 22-weeks old mice following conditional MECP knock-out at 12 weeks by RNA-sequencing. Consistent with previous data, we identify mild gene expression changes following MECP2 knock-out. These data could prove valuable in future studies comparing conditional MECP2 knock-out at distinct time points and in additional brain regions, and can also serve for investigating alternative splicing changes resulting from MECP2 conditional deletion.

2018-04-05 | GSE112663 | GEO

Adrenalectomy plus corticosterone treatment, rat hippocampal RNA-seq

Project description:Male Sprague-Dawley rats 8 weeks old, were adrenalectomized, treated with 300ug/kg corticosterone or vehicle 3 days after surgery then sacrificed 1 hour later. Hippocampi were removed and RNA extracted and processed for sequencing at the Massachusetts General Hospital Nex-Generation Sequening Core.

2016-08-11 | GSE84249 | GEO

MECP2 directly interacts with RNA polymerase II to modulate transcription in human neurons

Project description:This dataset comprises 15 raw AP-MS files, each with an associated peak list, captured using a Vanquish Neo nanoLC system in tandem with an Orbitrap Eclipse mass spectrometer. To generate MECP2 hESC-reporter lines for wild type (WT) and various mutations of MECP2, including R133C, R168X, and R270X, we first used CRISPR/Cas9 to create MECP2 alleles carrying the green fluorescent protein (GFP) sequences in the endogenous gene. The R133C mutation was then introduced into the WT MECP2-GFP reporter line. Mutations R133C, R168X, and R270X are recognized as loss-of-function variants in MECP2 and are also identified as primary Rett syndrome-causing mutations. For efficient neuronal differentiation, a doxycycline (DOX)-responsive NGN2 construct was incorporated at their AAVS1 safe harbor locus. Upon the addition of DOX, homogenous populations of neurons were generated within three weeks from those four MECP2 hESC-reporter lines. Subsequently, GFP-pull down assay and AP-MS were performed using these WT MECP2-GFP neurons along with R133C-, R168X-, and R270X-mutant MECP2-GFP reporter neurons. Neurons expressing only the GFP tag served as a negative control. AP-MS analysis identified proteins interacting differently between WT and mutant MECP2 within human neurons.

2023-10-27 | MSV000093210 | MassIVE

Hypothalamic gene expression data from Mecp2-null and MECP2-transgenic mice

Project description:We compared gene expression changes in the hypothalamus of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-transgenic). Mutations in the gene encoding the transcriptional repressor methyl-CpG binding protein 2 (MeCP2) cause the neurodevelopmental disorder Rett syndrome. Loss of function as well as increased dosage of MECP2 gene cause a host of neuropsychiatric disorders. To explore the molecular mechanism(s) underlying these disorders, we examined gene expression patterns in the hypothalamus of mice that either lack or overexpress MeCP2. In both models, MeCP2 dysfunction induced changes in the expression levels of thousands of genes, but surprisingly the majority of genes (~85%) appeared to be activated by MeCP2. We selected six genes and confirmed that MeCP2 binds to their promoters. Furthermore, we showed that MeCP2 associates with the transcriptional activator CREB1 at the promoter of an activated target but not a repressed target. These studies suggest that MeCP2 regulates the expression of a wide range of genes in the hypothalamus and that it can function as both an activator and repressor of transcription. Total hypothalamic RNA samples were collected from Mecp2-null male mice (n=4), MECP2-transgenic male mice (n=4), and their wild type male littermates at 6 weeks of age (n=4 for each group).

2008-05-30 | E-GEOD-11150 | biostudies-arrayexpress

Time-lapse hippocampal transcriptomic profiling after fear conditioning in Tob WT and KO mice

Project description:Fear conditioning induces immediate changes in the mouse hippocampal transcriptome profile. Here, we performed RNA sequqencing in mice hippocampi at 15 minutes, 1 hour and 3 hours post-fear conditioning in addition to non-conditioned mice. Tob gene has been shown to affect cellular stress and behavior. In order to understand the role of Tob gene in the hippocampal stress and fear machinery, we compared hippocampi of Tob WT and KO mice. This dataset shows the temporal transcriptomic changes in mouse hippocampus induced by fear conditioning. Also, it shows the changes occurred after Tob deletion.

2022-08-16 | GSE186101 | GEO

Transcriptomic analysis of adult mouse hippocampal tissue in control and MeCP2 knockdown conditions

Project description:The overall goal of this study was to clarify the role of MeCP2 in adult cognition. As one of the measures we analyzed gene expression changes associated with MeCP2 loss in the adult hippocampus. The analysis was performed in basal conditions and after exposure to a novel environment. We report gene expression data of mouse adult hippocampal tissue in which MeCP2 has been knockeddown in both conditions.

2018-05-15 | GSE107004 | GEO

Adrenalectomy plus corticosterone treatment, rat hippocampal RNA-seq

2016-08-11 | E-GEOD-84249 | biostudies-arrayexpress

Cerebellar gene expression data from Mecp2-null and MECP2-transgenic mice

Project description:We compared gene expression changes in the cerebellum of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-transgenic). A group of postnatal neurodevelopmental disorders collectively referred to as MeCP2 disorders are caused by aberrations in the gene encoding methyl-CpG-binding protein 2 (MECP2). Loss of MeCP2 function causes Rett syndrome (RTT), whereas increased copy number of the gene causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however the gene expression changes observed in the hypothalamus of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. To determine if this dual role of MeCP2 extends beyond the hypothalamus, we studied gene expression patterns in the cerebellum of Mecp2-null and MECP2-Tg mice, modeling RTT and MECP2 duplication syndrome, respectively. We found that abnormal MeCP2 dosage causes alterations in the expression of hundreds of genes in the cerebellum. The majority of genes were upregulated in MECP2-Tg mice and downregulated in Mecp2-null mice, consistent with a role for MeCP2 as a modulator that can both increase and decrease gene expression. Interestingly, many of the genes altered in the cerebellum, particularly those increased by the presence of MeCP2 and decreased in its absence, were similarly altered in the hypothalamus. Keywords: Comparison of cerebellar gene expression data between Mecp2-null mice and Mecp2-transgenic mice Total cerebellar RNA samples were collected from Mecp2-null male mice (n=5), MECP2-transgenic male mice (n=5), and their wild type male littermates at 6 weeks of age (n=5 for each group).

2010-04-10 | E-GEOD-15574 | biostudies-arrayexpress

RNA Sequencing on hippocampal tissue after ASO treatment overtime in MECP2 duplication mice

Project description:To understand the response of MECP2-regulated genes to the ASO treatment, we performed RNA-sequencing at multiple timepoints on hippocampal tissue following ASO treatment. It shows that the abnormal transcriptomic profile of hDup mice is significantly rescued 2 weeks after the treatment. Long-term partial rescue of the gene expression was observed at 5 weeks and until 16 weeks after the treatment as the transcriptomic profile does not cluster with the control-ASO treated mice.

2022-05-26 | GSE151222 | 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