Similar Datasets
Project description:In this study endothelial cells of the forebrain, cerebellum, spinal cord, lungs and liver were acutely purified by FACS. RNA-Seq was performed on isolated endothelial cells and their transcriptome was compared to identify regional blood-brain barrier specific transcripts.
2024-06-16 | GSE171105 | GEO
Project description:We generated single-cell RNAseq profiles of 143 microglia, sorted in the gate CD45lowCD11+Gpnmb+Clec7a+, from postnatal day 7 cerebellum to validate the newly identified “proliferative region-associated microglia (PAM)” (Gpnmb and Clec7a are PAM surface markers). Single cells were FACS index sorted followed by Smart-seq2 library preparation and Illumina Nextseq (sequence depth > 1 million per cell). These cells showed characteristic PAM gene expression and clustered together with other PAM cells sequenced in the same study.
2018-12-31 | GSE123024 | GEO
Project description:The goal of this experiement was to determine what transcriptional differences there are between P195A/p150- (sick) and P195A/p150+ (healthy) mice. Kidney, Liver, and Cerebellum were the most clearly affected on histology and qPCR for IFN. We found an IFN signature and ISR signature were both upregulated in P195A/p150- mice as compared to P195A/p150+ littermates.
2021-08-26 | GSE162583 | GEO
Project description:Transcriptional profiling to identify genes differentially regulated by Sufu during cerebellum development. Sufu was specifically deleted from the granule neuron compartment using Math1-driven Cre recombinase.
2020-01-15 | GSE143671 | GEO
Project description:We performed bulk RNA-seq on Nas2Del +/- Het and wild type postnatal Day 20 mice on samples collected from the mouse forebrain.
2021-04-10 | GSE171765 | GEO
Project description:A number of human neurodegenerative diseases result from the expansion of a glutamine repeat within the disease-causing protein. Spinocerebellar ataxia type1 is one such disease, caused by expansion of a polyglutamine tract in the novel protein ataxin-1. To faithfully model SCA1 in the mouse, we generated knock-in mice carrying 154 CAG repeats in the mouse Sca1 locus. These mice reproduced many aspects of the human disease. Despite ubiquitous expression of the mutant protein, they developed slowly progressive selective neurodegeneration , which is most distinct in Purkinje cells and spinal cord. Alterations in gene expression have been proposed to be involved in the pathogenesis of polyglutamine disease including SCA1, but the changes of gene expression in an authentic disease model have not been characterized. We believe that knowledge of these genes will give insight into the pathophysiology of SCA1 and may ultimately be relevant to the treatment of SCA1.,We will determine gene expression patterns in the cerebellum and forebrain at three different time points.,We propose that the genes whose expression is affected by mutant ataxin-1 expression are effectors for neuronal dysfunction and neuronal degeneration in the knock-in mice. We also hypothesize the difference in the expression levels of these genes accounts for selective vulnerability of neurons.,We will examine three time points: 4 weeks, 11 weeks, and 20 weeks of age. We have shown that the mice developed motor incoordination as revealed by rotating rod test as early as 5 weeks of age but it was not until 10 weeks that they start showing clear neurological phenotype such as clasping. At each point, we will compare the pattern between the mutant and wild-type littermate. Animals will be prepared and sacrificed by a standard procedure. Cerebellum and spinal cord are the most affected areas whereas forebrain shows less neurodegeneration. Tissue will be rapidly dissected from cerebellum and forebrain, frozen in liquid nitrogen, and stored at ?80 C until analysis. Tissues will be sent to the centers (as opposed to RNA). We will be providing 9 tissue samples from three litters for each time point to mitigate any expression differences resulting from subtle differences of procedure or environment where the mice grow.
2007-07-07 | E-GEOD-2867 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare Wild Type and EED-/- cerebellum transcriptome profiling (RNA-seq) to quantitative reverse transcription polymerase chain reaction (qRT–PCR) differentially expressed genes and find target genes. We performed chromatin-immunoprecipitation coupled to sequencing (ChIP-seq) to dissect the relationship between the differentially expressed genes and the occupancy of H3K27me3, H3K27ac and EED. Methods: Cerebellum mRNA profiles of 14-day-old(P14) wild-type (WT) and Embryonic Ectoderm Development conditional knockout (EED-/-) mice were generated by deep sequencing, in triplicate,using Illumina HiSeq 2500 system.All RNA-Seq data were aligned to mouse genome version mm10 using Salmon (v.1.1.0) .We use cluster software and Euclidean distance matrix for the hierarchical clustering analysis of the expressed gene and sample program at the same time, the clustering results can be viewed with javaTreeview. qRT–PCR validation was performed using SYBR Green assays. we performed ChIP-seq using freshly isolated P14 from Wild Type and EED-/- cerebellar tissues . DNA libraries generated from ChIP-DNA and input-DNA were deep-sequenced using HiSeq single-end 50bp. Results:Only transcripts that showed more than 1.5-fold differential expression compared to control were subjected to relevance network analysis. 3149 candidate genes that were differentially expressed with biological functional groups as compared between WT and EED-/- mice .We found that the enrichment of H3K27me3 was decreased H3K27ac was highly increased in EED-/- mice. Conclusions: Our study represents the first detailed analysis of Wild Type and EED-/ mice cerebellum transcriptomes, with three biologic replicates, generated by RNA-seq technology. We report the application of ChIP-sequencing technology for high-throughput profiling of histone modifications in cerebellar cells.
2024-04-02 | GSE169312 | GEO
Project description:Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by motor neuron degeneration. MATR3 is an ALS-linked gene that encodes an RNA-binding protein that is involved in alternative splicing regulation. S85C is the most commonly identified mutation in MATR3. We generated MATR3 S85C knock-in mice (of the C57BL/6 background) as a model to study ALS pathogenesis and we found that homozygous S85C mice begin to show phenotypes at around 10 weeks of age. To investigate the molecular changes that may contribute to the behavioural deficits and neurodegeneration observed in homozygous S85C mice, we performed RNA-seq on cortex, cerebellum and lumbar spinal cord tissue of wild-type, heterozygous and homozygous S85C mice (4 females per genotype) at the early symptomatic stage (8-10 weeks old). Total RNA was extracted and sent to SickKids TCAG core for mRNA library preparation, which were paired end (100 bp in length) sequenced on the Illumina NovaSeq S1 flow cell. The data obtained was aligned to mouse genome (mm10) using STAR aligner (v2.6.0), and paired-end reads mapping to exonic regions were counted using featureCounts (v1.6.3). Differential gene expression was analyzed using edgeR.
2020-08-18 | E-MTAB-8838 | biostudies-arrayexpress
Project description:A relatively small number of proneural transcription factors specify a multitude of neural progenitor populations in the developing mammalian brain. Despite their importance, little is known about their targets, cellular processes they regulate, or what genomic sites they occupy in vivo. We used an integrated experimental and computational approach, combining RNA-seq, Histone-seq, and Atoh1 ChIP-seq in cerebellar tissue, to identify over 600 targets of Atoh1, an important developmental transcription factor. We validated 10% of these targets and found that Atoh1 directly regulates genes involved not only in early proliferation but also later differentiation, migration, cell adhesion, metabolism, and cytoskeletal organization by recognizing a novel 10 nucleotide Atoh1 E-Box associated motif (AtEAM). This Atoh1 “targetome” is not only a resource for studies aimed at understanding the molecular mechanisms involved in cerebellar development, but our integrated approach provides a framework for future in vivo studies of transcription factors and their targetomes. Examination of RNA-seq WT and null expression data (2 reps each), 2 different histone modifications (2 rep each) and IgG control, and Atoh1 DNA-binding (2 reps each) and control in the developing cerebellum
2011-02-08 | E-GEOD-22111 | biostudies-arrayexpress
Project description:Transcriptome analysis of Ts1Cje (mouse model of Down syndrome) and euploids murine cerebellum during postnatal development Keywords = Down syndrome Keywords = Chromosome 21 Keywords = Transcriptome Keywords = Microarray Keywords = Cerebellum Keywords = Development Keywords: other
2004-12-05 | E-GEOD-1611 | biostudies-arrayexpress