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Single cell ATAC-seq analysis in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene (10X Genomics Multiome)

ABSTRACT: Single cell ATAC-seq analysis in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene (10X Genomics Multiome)

PROVIDER: PRJNA975137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24686813.fastq.gz	Fastqsanger.gz
	SRR24686813_1.fastq.gz	Fastqsanger.gz
	SRR24686813_2.fastq.gz	Fastqsanger.gz
	SRR24686814.fastq.gz	Fastqsanger.gz
	SRR24686814_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq of the human fetal neocortex, lateral ganglionic eminence and medial ganglionic eminence at 7, 9, 11 and 20 post-conceptional weeks

Project description:Deep transcriptional profiling of the human neocortex, lateral ganglionic eminence (LGE) and medial ganglionic eminences (MGE), from 7 to 20 post-conceptional weeks (pcw), for de novo lincRNAs discovery and to establish a unique coding and non-coding gene signature for the three different regions.

2021-05-13 | E-MTAB-8893 | biostudies-arrayexpress

Expression data from purified medial ganglionic eminence (MGE) interneurons, 3 biological replicates

Project description:During development, newborn interneurons migrate throughout the embryonic brain. Here, we provide evidence that these interneurons act in a paracrine fashion to regulate developmental oligodendrocyte formation. Specifically, we show that medial ganglionic eminence (MGE) interneurons secrete factors that promote genesis of oligodendrocytes from glially-biased cortical precursors in culture. Moreover, when MGE interneurons are genetically ablated in vivo prior to their migration, this causes a deficit in cortical oligodendrogenesis. Modeling of the interneuron-precursor paracrine interaction using transcriptome data identifies the cytokine fractalkine as responsible for the pro-oligodendrocyte effect in culture. This paracrine interaction is important in vivo, since knockdown of the fractalkine receptor CX3CR1 in embryonic cortical precursors, or constitutive knockout of CX3CR1 causes decreased numbers of oligodendrocyte progenitor cells (OPCs) and oligodendrocytes in the postnatal cortex. Thus, in addition to their role in regulating neuronal excitability, interneurons act in a paracrine fashion to promote the developmental genesis of oligodendrocytes. We used microarrays to generate a list of expressed genes in purified medial ganglionic eminence (MGE) interneurons

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CTCF occupancy in the mouse telencephalon and medial ganglionic eminence

Project description:In this study, we wanted to compare CTCF binding sites in whole telencephalon vs medial ganglionic eminence (MGE) at embryonic day E13.5.

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Single cell RNA-seq analysis in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene (10X Genomics Multiome)

Project description:Enhancer of zeste homolog 2 (Ezh2) is the methyltransferase component of the Polycomb Repressive Complex 2 (PRC2), which is critical for trimethylation of histone 3 at lysine 27 (H3K27me3) and results in gene repression. Mutations in EZH2 and dysregulation of H3K27me3 can lead to neurodevelopmental abnormalities such as Weaver Syndrome and ataxia-telangiectasia. During cortical neurogenesis, H3K27me3 is a critical epigenetic modification that regulates cellular maturation rate, and in turn, determines when precursor cells exit the cell cycle. Loss of function studies reveal that Ezh2 plays a critical role in epigenetic regulation of neuronal fate and maturation in some brain regions, but a role for Ezh2 in forebrain GABAergic interneurons has not been explored. Here, we removed Ezh2 from the medial ganglionic eminence (MGE) to study its role in interneuron development.

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Single cell ATAC-seq analysis in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene (10X Genomics Multiome)

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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.

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Single cell 10X Genomics Multiome analysis in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene

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RNA-seq of laser-capture microdissected 50x50x50 um tissue cubes from the medial ganglionic eminence of wild-type and GFRa1 mutant mice

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Effect of depletion of Rac1 and Rac3 GTPases on gene expression in cells from the medial ganglionic eminence (MGE)

Project description:Το investigate the role of Rac1 and Rac3 GTPases in the development of MGE-derived cortical interneurons we generated a transgenic mice where both Rac1 and 3 were depleted from the medial ganglionic eminence. First we generated a conditional knockout for Rac1 (Vidaki et al. 2012) by crossing animals carrying a floxed allele of Rac1 (Rac1fl/fl) (the fourth and fifth exon of the Rac1 gene are flanked with loxP sites, Walmsley et al. 2003) to the Nkx2.1Tg(Cre) mice (Nkx2.1 transgenic Cre, Fogarty et al. 2007). The ROSA26fl-STOP-fl-YFP allele was also inserted as an independent marker (Srinivas et al. 2001). Next, we crossed the Rac1 conditional knockout with the Rac3 KO line (Corbetta et al. 2005) and obtained a mouse line where Rac1 and Rac3 were both depleted from the MGE-derived interneurons.

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CUT&Tag analysis on H3K27me3 in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene

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