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Mus musculus

ABSTRACT: Transcriptome analysis of cortical PV cells during brain development in wild-type and Nipbl mutant mice

PROVIDER: PRJDB9258 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR205683.fastq.gz	Fastqsanger.gz
	DRR205684.fastq.gz	Fastqsanger.gz
	DRR205685.fastq.gz	Fastqsanger.gz
	DRR205686.fastq.gz	Fastqsanger.gz
	DRR205687.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Analysis of regulatory landscape of chromatin in cortical PV-cells during brain development in wild-type and Nipbl mutant mice

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Mus musculus

Project description:Analysis of regulatory landscape of chromatin in cortical PV-cells during brain development in wild-type and Nipbl mutant mice

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Mus musculus

Project description:Transcriptome analysis of cortical excitatory neurons of juvenile brain in wild-type and Nipbl mutant mice

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Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [single-cell RNA-seq]

Project description:Purpose: To gain futher insight into how STING causes abnormal cortical development in mice ,single cell RNA-seq was used to analyze the cell type changes resulting from the cerebral cortices of P0 STING conditional knock out mice and littermate wild-type. Methods: Single cell isolation was prepared from P0 telencephalic tissue of wild-type(WT) and STINGf/f;Nestin-Cre mice. The fragmented cDNAs containing barcode and UMI sequences was built the library . Agilent 2100 Bioanalyze was used to quality controlled and quantified.Single cell RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Clustering and labeling of these cells visualized on a t-SNE plot between the wild-type(WT) and STINGf/f;Nestin-Cre mice brain cortex Conclusions: Single cell RNA-seq data would provide a overall understanding of how STING gene influences cortical development in mice.

2020-03-06 | GSE146456 | GEO

Sp9 regulates medial ganglionic eminence-derived cortical interneuron development

Project description:In the mammalian cortex, about 60% of GABAergic interneurons, mainly including parvalbumin-expressing (PV+) and somatostatin (SST+) interneurons are generated from the medial ganglionic eminence (MGE) in the subpallium and tangentially migrate to the cortex. Here we analyze the role of the Sp9 transcription factor in regulating the development of MGE-derived cortical interneurons. We show that SP9 is widely expressed in the MGE subventricular zone (SVZ) and in MGE-derived migrating interneurons. By analyzing Sp9 null and conditional mutant mice, we demonstrate that Sp9 promotes MGE progenitor proliferation in the SVZ and is required for the normal patterning of tangential migration and the laminar distribution of MGE-derived cortical GABAergic interneurons. Loss of Sp9 function results in a ~50% reduction of MGE-derived cortical interneurons, an ectopic aggregation of MGE-derived neurons in the embryonic ventral telencephalon, and an increased ratio of SST+/PV+ cortical interneurons. Finally, we provide evidence that Sp9 regulates MGE derived cortical interneuron development through promoting expression of the Lhx6 and Lhx8 transcription factors.

2017-05-19 | GSE99049 | GEO

Gene expression profile at single cell level of mouse cortical brain cells

Project description:We used single cell RNA sequencing (scRNA-seq) to compare cortical brain cells from mast cell wild-type with mast cell knockout mice.

2023-08-20 | GSE240687 | GEO

Transcriptome analysis of rice ABA deficient mutant Osaba1-1 and wild-type before and 72h after Xanthomonas oryzae pv. oryzae (Xoo) infection

Project description:ABA deficient mutant Osaba1-1 exhibits great resistance to Xanthomonas oryzae pv. oryzae (Xoo) infection. To investigate gene expression profile changes at whole genome level between Osaba1-1 and wild-type (Nipponbare) rice during Xoo infection, we employed microarray expression profiling as a discovery platform.

2015-05-15 | GSE63337 | GEO

RNA-seq of primary dissociated cortical Nipbl+/- neurons

Project description:RNA-seq of total RNA from Nipbl+/+ and Nipbl+/- dissociated cortical neurons at Day In Vitro (DIV10)

2021-02-28 | GSE161796 | GEO

Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [bulk RNA-seq]

Project description:Purpose: To gain futher insight into how STING regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E13 STING conditional knock out mice and littermate wild-type. Methods: Total RNA from E13 telencephalic tissue of wild-type(WT) and STINGf/f;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and STINGf/f;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the down or up-regulated genes showed obvious enrichment of biological processes related to brain development and cell fate commitment. These results reflected STING plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how STING gene contribute to brain cortical development.

2020-03-06 | GSE146455 | GEO

Cell-specific vulnerability to metabolic failure: the crucial role of parvalbumin expressing neurons in creatine transporter deficiency

Project description:Mutations in the solute carrier family 6-member 8 (Slc6a8) gene, encoding the protein responsible for cellular creatine (Cr) uptake, cause Creatine Transporter Deficiency (CTD), an X-linked neurometabolic disorder presenting with intellectual disability, autistic-like features, and epilepsy. The pathological determinants of CTD are still poorly understood, hindering the development of therapies. In this study, we generated an extensive transcriptomic profile of CTD showing that Cr deficiency causes perturbations of gene expression in excitatory neurons, inhibitory cells, and oligodendrocytes which result in remodeling of circuit excitability and synaptic wiring. We also identified specific alterations of parvalbumin-expressing (PV+) interneurons, exhibiting a reduction in cellular and synaptic density, and a hypofunctional electrophysiological phenotype. Mice lacking Slc6a8 only in PV+ interneurons recapitulated numerous CTD features, including cognitive deterioration, impaired cortical processing and hyperexcitability of brain circuits, demonstrating that Cr deficit in PV+ interneurons is sufficient to determine the neurological phenotype of CTD. Moreover, a pharmacological treatment targeted to restore the efficiency of PV+ synapses significantly improved cortical activity in Slc6a8 knock-out animals. Altogether, these data demonstrate that Slc6a8 is critical for the normal function of PV+ interneurons and that impairment of these cells is central in the disease pathogenesis, suggesting a novel therapeutic venue for CTD.

2023-03-14 | GSE216766 | GEO

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