TRAP-seq from hippocampus isolated from WT and Fmr1-/y mice bred to Snap25-EGFPL10a mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE199328 | GEO | 2022/06/07
REPOSITORIES: GEO
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Project description:TRAP-seq from hippocampus isolated from WT and Fmr1-/y mice bred to Snap25-EGFPL10a mice
| PRJNA819407 | ENA
Project description:TRAP (translating ribosome affinity purification) from CA1 pyramidal neurons and cerebellar granule cells in wildtype and Fmr1 KO littermate pairs. These data show a global downregulation of FMRP targets in Fmr1 KO mice in these cell types.
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Project description:The Fragile X Mental Retardation Protein, FMRP, is thought to regulate the translation of a specific set of neuronal mRNAs on polyribosomes. Therefore, we prepared polyribosomes on sucrose gradients and purified mRNA specifically from these fractions, as well as the total mRNA levels, to determine whether a set of mRNAs might be changed in its % association with polyribosomes in the absence of FMRP in the KO mouse model. No significant differences were found, other than the Fmr1 transcript itself, in total mRNA levels or % polyribosome association that withstood multiple test correction, in P7 Fmr1 KO mouse cerebral cortex compared with WT littermates.. We prepared polyribosomes on sucrose gradients from 6 littermate pairs of Fmr1 KO and WT littermates (FVB background, P7 males, cerebral cortex) and purified RNA from both polyribosomal fractions and input to the gradient, reflecting total mRNA levels for comparison.
2011-07-20 | E-GEOD-26745 | biostudies-arrayexpress
Project description:The molecular mechanism(s) leading to Purkinje neuron loss in the neurodegenerative disorder Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS) are limited by the complex morphology of this cell type. Purkinje neurons are notoriously difficult to isolate and maintain in culture presenting considerable difficultly to identify molecular changes in response to riboCGG repeat-containing mRNA that induces neurotoxicity in FXTAS. Several studies have uncovered a number of RNA binding proteins involved in translation that aberrantly interact with the toxic RNA; however, whether these interactions alter the translational profile of cells has not been investigated. Here we employ bacTRAP translational profiling to demonstrate that Purkinje neurons ectopically expressing 90 CGG repeats exhibit a dramatic change in their translational profile even prior to the onset of riboCGG-induced phenotypes. This approach identified nearly 500 transcripts that are differentially associated with ribosomes in r(CGG)90-expressing mice. Functional annotation cluster analysis revealed broad ontologies enriched in the r(CGG)90 list, including RNA binding and response to stress. Intriguingly, a transcript for the Tardbp gene, implicated in a number of other neurodegenerative disorders, exhibits altered association with ribosomes in the presence of r(CGG)90 repeats. We therefore tested and showed that reduced association of Tardbp mRNA with the ribosomes results in a loss of TDP-43 protein expression in r(CGG)90–expressing Purkinje neurons. Furthermore, we showed that TDP-43 could modulate the rCGG repeat-mediated toxicity in a Drosophila model that we developed previously. These findings together suggest translational dysregulation may be an underlying mechanism of riboCGG-induced neurotoxicity and provide insight into the pathogenicity of FXTASBAC-trap studies of Purkinje cels in normal and mutant mice Looking for cell type specific gene expression differences caused by mutation in FMR1 using BAC-Trap RNA capture assay. A cutoff value of 4.5 for mean probe_set mean across all 18 hybridizations was used to determine a cutoff for expression in Purkinje cells. This 16040 corresponded to a mean value of at least 3.4323 in the 4week time point. L7CGG90Fmr1:Pcp2 BAC (r(CGG)90 BAC) and wild-type:L7/Pcp2 BAC (WT BAC) transgenic mice used in this study have a 50% C57B6 and 50% FVB genetic background and were derived from the same parents by crossing L7CGG90Fmr1 heterozygote transgenics (100% C57B6 background) with L7/Pcp2eEGFPL10a BAC homozygous transgenics (100% FVB background). All mice reported were F1 progeny and were therefore hemizygous for one or both transgenes. Littermate wild-type mice were used for all experiments whenever possible.
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Project description:To better understand the effects silencing the Fmr1 gene, we conducted an integrative analysis of learning behavior, synaptic physiology, and hippocampal gene expression.
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Project description:Zinc finger protein ZBTB20 plays a critical role in mouse hippocampal development by orchestrating gene expression profile of hippocampal neurons. We used microarrays to investigate the target gene of ZBTB20 in mouse hippocampal development. Mouse hippocampi were harvested at postnatal day 2 for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify the target genes of transcription factor ZBTB20 in hippocampal development. To that end, we isolated the hippocampi from ZBTB20 knockout and their littermate control mice.
2010-03-08 | E-GEOD-19513 | biostudies-arrayexpress
Project description:Transgenic mouse lines that express His6-SUMO1 and His6-SUMO2 under the control of the neuron specific Thy1.2 promoter were generated and characterized. The effect of increased levels of SUMO1 and -2 at the level of gene expression in the hippocampus was studied. Pooled (left and right) hippocampi were dissected from adult littermate wild-type control (WT1) and SUMO1 and WT2 and SUMO2 transgenic animals (n=3) and subjected to RNA expression analysis.
2013-12-31 | E-GEOD-47951 | biostudies-arrayexpress
Project description:Fragile X syndrome (FXS) is the most common monogenetic cause of inherited intellectual disability and autism in humans. One of the well-characterized molecular phenotypes of Fmr1 KO mice, a model of FXS, is increased translation of synaptic proteins. Although this upregulation stabilizes in the adulthood, abnormalities during the critical period of plasticity have long-term effects on circuit formation and synaptic properties. Using high-resolution quantitative proteomics of synaptoneurosomes isolated from the adult, developed brains of Fmr1 KO mice, we show differential abundance of proteins regulating postsynaptic receptor activity of glutamatergic synapse. This work includes proteomic dataset that was acquired and analyzed to quantify changes in the abundance of proteins in synaptoneurosomes (basal state, unstimulated and in vitro NMDA-R stimulated) isolated from Fmr1 KO mice and their wild-type littermates.
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