Cerebellar RNA in Grid2 deficient mice.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE55314 | GEO | 2014/02/26
SECONDARY ACCESSION(S): PRJNA239309
REPOSITORIES: GEO
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Project description:Downsream of GRID2 in the mouse cerebellum. Control mice N=3 and Grid2 deficient mouse N=3
2014-02-26 | E-GEOD-55314 | biostudies-arrayexpress
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2010-05-27 | E-GEOD-2 | biostudies-arrayexpress
Project description:Gb5 is a divergent, evolutionarily-conserved, member of the heterotrimeric G protein b subunit family that is expressed principally in brain and neuronal tissue. Among Gb isoforms, Gb5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling (RGS) proteins that contain G protein-g like (GGL) domains. Previous studies employing Gb5 knockout mice have shown that Gb5 is an essential stabilizer of GGL domain-containing RGS proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. The purpose of this study is to better understand the functions of Gb5 in the brain outside the visual system by employing molecular biology, immunohistochemistry and confocal imaging technologies. We show here that mice lacking Gb5 have a markedly abnormal neurologic phenotype that includes neurobehavioral developmental delay, wide-based gait, motor learning and coordination deficiencies, and hyperactivity. Using immunohistochemical analysis and a green fluorescent reporter of Purkinje cell maturation we show that the phenotype of Gb5-deficient mice includes, in part, delayed development of the cerebellar cortex, an abnormality that likely contributes to the neurobehavioral phenotype. Multiple neuronally-expressed genes are dysregulated in cerebellum of Gb5 KO mice.
2011-09-13 | GSE29081 | GEO
Project description:Gb5 is a divergent, evolutionarily-conserved, member of the heterotrimeric G protein b subunit family that is expressed principally in brain and neuronal tissue. Among Gb isoforms, Gb5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling (RGS) proteins that contain G protein-g like (GGL) domains. Previous studies employing Gb5 knockout mice have shown that Gb5 is an essential stabilizer of GGL domain-containing RGS proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. The purpose of this study is to better understand the functions of Gb5 in the brain outside the visual system by employing molecular biology, immunohistochemistry and confocal imaging technologies. We show here that mice lacking Gb5 have a markedly abnormal neurologic phenotype that includes neurobehavioral developmental delay, wide-based gait, motor learning and coordination deficiencies, and hyperactivity. Using immunohistochemical analysis and a green fluorescent reporter of Purkinje cell maturation we show that the phenotype of Gb5-deficient mice includes, in part, delayed development of the cerebellar cortex, an abnormality that likely contributes to the neurobehavioral phenotype. Multiple neuronally-expressed genes are dysregulated in cerebellum of Gb5 KO mice. Brain tissues from WT and KO with three biological replications of mice were collected, frozen in liquid nitrogen, and stored at -70 °C
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Project description:We used a custom Affymetrix GeneChip, the "GLYCOv2" array, to measure differences in gene expression patterns from adult and postnatal day 7 (P7) mouse cerebellum RNA. Keywords = Cerebellum, microarray, development, glycoconjugates, glycosyltransferases, proteoglycans, gene expression Keywords: other
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Project description:Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS) is caused by mutations in SACS gene encoding sacsin. ARSACS patients and mouse models display early degeneration of cerebellum in agreement with high sacsin expression in this organ. We performed unbiased transcriptomic of cerebella from Sacs KO mice versus controls to dissect the mechanisms underlying cerebellar degeneration in ARSACS.
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Project description:We have recently discovered that deletion of Ptpn11, which codes for protein tyrosine phosphatase Shp2, blocks Bergmann glia (BG) formation and cerebellar foliation, whereas expressing a constitutively active Mek1 (Map2k1), Mek1DD, reverses the Ptpn11-deficient phenotypes, uncovering a previously unappreciated role of BG in folding of the cerebellar cortex. Relatively little is known regarding to the BG induction. The goal of the study was to determine molecular features of newly generated BG. To identify transcripts enriched in nascent BG, we performed RNA-seq of microdissected cerebellar tissues from wild type (WT), En1cre/+;Ptpn11F/F (Ptpn11-cKO), and En1cre/+;Ptpn11F/F;R26Mek1DD/+ (Ptpn11-cKO;MEK) embryos at E12.5, E13.5, and E14.5. As BG are initially formed at E13.5, we reasoned that BG-enriched transcripts should be increased from E12.5 to E14.5, decreased in Ptpn11-cKO cerebella, and restored in Ptpn11-cKO;MEK cerebella. By intersecting differentially expressed (DE) genes based on the above-mentioned assumptions, we wanted to identify genes that are specifically expressed in BG and affected by Ptpn11 deletion. Conclusions: though RNA-seq and subsequent validation, we have successfully identified genes that enriched in nascent BG in the developing mouse cerebellum.
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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
2009-04-07 | GSE15574 | GEO
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).
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