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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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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

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

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.

2021-07-26 | GSE171344 | GEO

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

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

2012-12-08 | E-MTAB-893 | biostudies-arrayexpress

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

2021-07-26 | GSE171343 | GEO

RNA-binding proteins Cugbp1 and HuD regulate neocortical projection neuron identities under the translational control of Neurotrophin-3

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

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.

2019-08-21 | GSE133912 | GEO

Glutamatergic dysfunction precedes neuron loss in cerebral organoids with MAPT mutations

Project description:Glutamatergic dysfunction precedes neuron loss in cerebral organoids with MAPT mutations

| PRJNA719153 | ENA

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

Project description:Glutamatergic dysfunction precedes neuron loss in cerebral organoids with MAPT mutations [scRNA-Seq]

| PRJNA719158 | ENA

Foxp1 drives striatal projection neuron specification and organization via cell-type specific mechanism

Project description:The molecular mechanisms that underlie striatal development and organization remain largely unknown. Here, we show that Foxp1, a transcription factor strongly linked to autism and intellectual disability, regulates organizational features of striatal circuitry in a cell-type dependent fashion. Using single-cell RNA-sequencing, we examine the cellular diversity of the early postnatal striatum and demonstrate that Foxp1 specifies a subpopulation of indirect pathway spiny projection neurons (iSPNs) while maintaining the striosome-matrix architecture through molecular mechanisms mediated by direct pathway spiny projection neurons (dSPNs). Functionally, Foxp1 alters striatal projection patterns both cell-autonomously and non-autonomously. We connect these changes in striatal circuitry to distinct behavioral deficits relevant to phenotypes described in patients with FOXP1 loss-of-function mutations. These data reveal novel cell-type specific transcriptional mechanisms underlying distinct features of striatal circuitry and identify Foxp1 as a key regulator of striatal development

2020-04-13 | GSE125290 | GEO

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