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Effect of RFX3 or RFX4 knockdown on ventral telencephalic medial ganglionic eminence-like (MGE-like) neuronal precursors

ABSTRACT: Effect of RFX3 or RFX4 knockdown on ventral telencephalic medial ganglionic eminence-like (MGE-like) neuronal precursors

PROVIDER: PRJNA999244 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25443266_1.fastq.gz	Fastqsanger.gz
	SRR25443266_2.fastq.gz	Fastqsanger.gz
	SRR25443267_1.fastq.gz	Fastqsanger.gz
	SRR25443267_2.fastq.gz	Fastqsanger.gz
	SRR25443268_1.fastq.gz	Fastqsanger.gz

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Effect of RFX3 or RFX4 knockdown on ventral telencephalic medial ganglionic eminence-like (MGE-like) neuronal precursors

Project description:RFX3 and RFX4 were defined as transcription factors (TFs) with enriched TF binding sites in cis-regulatory elements that are activated during the conversion of human embryonic stem cells (hESCs) into ventral telencephalic MGE-like patterned neuronal precursors. Therefore, we conducted CRISPRi-mediated knockdown of RFX3 or RFX4 and profiled changes in gene expression in MGE-like ventral telencephalic progenitors by RNA-seq. This analysis revealed that RFX3 and RFX4 play important roles in cortical interneuron development, specifically during the transition from mitotically cycling neuronal precursors into post mitotic neurons.

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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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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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