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Sequential regulation of glutamatergic and subtype-specific projection neuron identities in the developing cerebral cortex

ABSTRACT: Sequential regulation of glutamatergic and subtype-specific projection neuron identities in the developing cerebral cortex

PROVIDER: PRJNA596452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10729922_1.fastq.gz	Fastqsanger.gz
	SRR10729922_2.fastq.gz	Fastqsanger.gz
	SRR10729923_1.fastq.gz	Fastqsanger.gz
	SRR10729923_2.fastq.gz	Fastqsanger.gz
	SRR10729924_1.fastq.gz	Fastqsanger.gz

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Sequential regulation of glutamatergic and subtype-specific projection neuron identities in the developing cerebral cortex

Project description:Purpose:To asses changes in gene expression profiles of cortices from the P0 wild type littermate controls and Tle4-/- null mutant mice. Methords:Total RNA was isolated and sequenced using an illumina high-seq 2500. Raw data was analyzed using TopHat. Genes were considered significantly changed whicn perform P value <= 0.05 Results: Compared to controls, 306 genes were significantly down-regulated in the Tle4 null mutant mice, and 338 genes were significantly up-regulated in the Tle4 null mutant mice.

2019-12-18 | GSE142269 | GEO

Foxp1 regulates the development of glutamatergic synaptic input onto spiny projection neurons expressing Drd2 [snRNA-seq]

Project description:Long-range glutamatergic inputs from the cortex and thalamus provide important motor and cognitive information to the striatum where they are integrated for learning and action planning. Genetic programs and transcription factors that orchestrate the development of these inputs are relatively unknown. The transcription factor, FOXP1, is crucial for the development of spiny projection neurons (SPNs) in the striatum. We investigated the cell-specific role of Foxp1 in the formation of glutamatergic inputs – including corticostriatal inputs. Embryonic Foxp1 deletion in dopamine receptor 2-expressing SPNs (D2 Foxp1cKO) leads to reduced transmission of corticostriatal excitatory inputs and decreased synaptically driven excitability. Postnatal deletion of Foxp1 also resulted in decreased glutamatergic inputs onto D2 SPNs. Single nuclei RNA sequencing of D2 Foxp1cKO striatum identified downregulated postsynaptic genes, consistent with the synaptic phenotype. Reinstating Foxp1 postnatally rescued electrophysiological deficits and expression of a subset of genes that were altered by embryonic deletion in D2 SPNs. Postnatal Foxp1 reinstatement could also rescue behavioral phenotypes. In summary, we demonstrate that FOXP1 regulates the development of corticostriatal circuitry. Further, changes at multiple levels of brain function resulting from loss of Foxp1 are rescued with postnatal Foxp1 reinstatement, indicating a therapeutic approach for individuals with FOXP1 syndrome.

2024-02-20 | GSE243662 | GEO

Single-cell atlas of thalamic projection systems

Project description:We collected single-cell RNAseq data from neurons of five thalamocortical projection systems (motor, somatosensory, visual, auditory, and prefrontal). Cells of each projection system were retrogradely labeled from their cortical target area, microdissected, and collected individually. By combining single-cell transcriptomics with in situ RNA hybridization, we found heterogeneity not only between thalamic nuclei but also within nuclei, with graded transitions between cell identities.

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Single cell sequencing and retrograde barcode tracing reveal human DA neuron identities based on projection patterns in stem cell-derived grafts

Project description:Groundbreaking research in the last decade has definitively established human pluripotent stem cells (hPSCs) as a powerful source for the unlimited generation of dopamine (DA) neurons used in cell-based therapy in Parkinson’s disease (PD). However, DA neurons constitute a heterogeneous group of cells with different molecular identities and, consequently, different functions and innervation targets. Moreover, the inaccessibility of the human brain has so far hindered our understanding of the highly complex human DA system and, therefore, the design of DA neuron subtype-specific differentiation protocols for more effective cell replacement therapies. Currently, DA neurons – located in human ventral midbrain – can only be reliably distinguished based on their projection patterns. Here, we used hPSCs to derive and then transplant DA neurons into a rat model of PD. After one year of transplantation, we performed single nucleus RNA sequencing (snRNAseq) of ~80,000 human nuclei to transcriptionally define cell type composition and obtained a comprehensive map of DA neuron molecular identities. Exploiting the fact that transplanted DA neurons innervated and integrated within the host circuitry, we then combined snRNAseq with axonal retrograde AAV barcoding to trace the projection patterns of molecularly distinct human DA neuron subtypes in the grafts. We thus defined human DA neuron transcriptional profiles based on their target-specific outgrowth in the host brain. The resulting datasets provide an unprecedented resource both for elucidating the molecular basis of human DA neuron diversity as well as for developing more targeted cell-based therapies, with major implications for outcomes of PD patients.

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Foxp1 regulates the development of glutamatergic synaptic input onto spiny projection neurons expressing Drd2 [snRNA-seq]

Project description:Foxp1 regulates the development of glutamatergic synaptic input onto spiny projection neurons expressing Drd2 [snRNA-seq]

| PRJNA1019347 | ENA

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Project description:Intrinsic molecular pathways in the central nervous system dictate neuronal cell fate during development. However, interplay of RNA binding proteins (RBPs) dictating mRNA translation, and their spatiotemporal extracellular regulators in neocortical neural stem cells during neurogenesis are poorly understood. Using an unbiased RNAseq screen of polysomes between early and mid-neurogenesis, we identified functionally related mRNA groups and their isoforms are regulated translationally in prenatal neocortices, including mRNAs encoding RBPs. Here, we show that isoforms of the RBP, Hu antigen D (HuD), regulate the balance of neocortical glutamatergic neurons in an isoform-specific manner during development. HuD3 promoted a Cdp+ intracortically projecting neuronal fate, while HuD4 promoted a Tle4+ subcortically projecting neuronal fate. In early neurogenic radial glia of the neocortex, HuD transcripts were bound and translationally repressed by another RBP, CUG triplet repeat RNA-binding protein 1 (Cugbp1). Cugbp1 knockdown increased the number of Cdp+ intracortically projecting neurons, while having distinct effects on Tle4+ and Ctip2+ subcortically projecting neurons. Neurotrophin-3 promoted HuD3 mRNA translation and Cdp+ fate, which was reversed by Cugbp1. Thus, our findings reveal a novel post-transcriptional molecular pathway in the developing neocortex that regulates the balance of distinct subpopulations of neocortical projection neurons.

2017-09-08 | GSE77647 | GEO

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Project description:Frontotemporal dementia (FTD) due to MAPT mutation causes pathological accumulation of tau and glutamatergic cortical neuronal death by unknown mechanisms. We used human induced pluripotent stem cell (iPSC)-derived cerebral organoids expressing tau-V337M and isogenic corrected controls to discover early alterations due to the mutation that precede neurodegeneration. Mutant organoids show early upregulation of MAPT expresssion and glutamatergic signaling pathways, as well as regulators including the RNA-binding protein ELAVL4. By 6 months, tau-V337M organoids show specific loss of glutamatergic neuronsof layers affected in patients. Mutant neurons are susceptible to glutamate toxicity, which was rescued pharmacologically by treatment with the PIKFYVE kinase inhibitor apilimod. Our results demonstrate a sequence of events that precede cell death, revealing molecular pathways associated with glutamate signaling as potential targets for therapeutic intervention in FTD.

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Glutamatergic dysfunction precedes neuron loss in cerebral organoids with MAPT mutations [bulk RNA-Seq]

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Gene expression profiles of glutamatergic neuron progenitors (Neurod6-positive cells)

Project description:Gene expression profiles of glutamatergic neuron progenitors (Neurod6-positive cells)

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Transcription profiling of mouse FACS-purified cortical projection neurons

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