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Gene expression profile of primary cortical neurons from necdin-null mouse embryo

ABSTRACT: Necdin, a pleiotropic protein expressed predominantly in postmitotic neurons of mammals, regulates neuronal development and survival by interacting with various regulatory proteins. To understand a novel function of necdin, we analyzed gene expression profile of primary cortical neurons prepared from necdin-null mice at embryonic day 14.5.

ORGANISM(S): Mus musculus

PROVIDER: GSE63498 | GEO | 2016/03/10

SECONDARY ACCESSION(S): PRJNA268071

REPOSITORIES: GEO

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Gene expression profile of primary cortical neurons from necdin-null mouse embryo

Project description:Necdin, a pleiotropic protein expressed predominantly in postmitotic neurons of mammals, regulates neuronal development and survival by interacting with various regulatory proteins. To understand a novel function of necdin, we analyzed gene expression profile of primary cortical neurons prepared from necdin-null mice at embryonic day 14.5. Wild-type and necdin-null cortical cells were prepared from mice at embryonic day 14.5. These cells were incubated in Neurobasal medium supplemented with B27 and differentiated into neurons for 4 days (>97% MAP2-positive postmitotic neurons). Three mice per genotype were used for analysis.

2016-03-10 | E-GEOD-63498 | biostudies-arrayexpress

Early emergence of cortical interneuron diversity in the mouse embryo

Project description:GABAergic interneurons play crucial roles in the regulation of neural circuit activity in the cerebral cortex. A hallmark of cortical interneurons is their remarkable structural and functional diversity, yet the molecular determinants and the precise timing underlying their diversification remain largely unknown. Here we use single-cell transcriptomics to identify distinct types of progenitor cells and newborn neurons in the ganglionic eminences, the embryonic proliferative regions that give rise to cortical interneurons. These embryonic precursors define temporally and spatially restricted transcriptional trajectories that unambiguously relate to specific classes of interneurons in the adult cerebral cortex. Our findings therefore suggest that interneuron diversity is already patent shortly after neurons become postmitotic through the acquisition of specific transcriptional programs that unfold over several weeks in the developing cortex

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Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway II

Project description:Developmental neuron death plays a pivotal role in refining organization and wiring during neocortex formation. Aberrant regulation of this process results in neurodevelopmental disorders including impaired learning and memory. Underlying molecular pathways are incompletely determined. Loss of Bcl11a in cortical projection neurons induces pronounced cell death in upper-layer cortical projection neurons during postnatal corticogenesis. We used this genetic model to explore genetic mechanisms by which developmental neuron death is controlled. Unexpectedly, we found Bcl6, previously shown to be involved in transition of cortical neurons from progenitor to postmitotic differentiation state to provide a major check point regulating neuron survival during late cortical development. We show that Bcl11a is a direct transcriptional regulator of Bcl6. Deletion of Bcl6 exerts death of cortical projection neurons. In turn, reintroduction of Bcl6 into Bcl11a mutants prevents induction of cell death in these neurons. Together, our data identify a novel Bcl11a/Bcl6-dependent molecular pathway in regulation of developmental cell death during corticogenesis.

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Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway I

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DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

Project description:Our group has reported that the histone methyltransferase DOT1L is necessary for proper cortical plate development and layer distribution of glutamatergic neurons, however, its specific role on cortical interneuron development has not yet been explored. Here, we demonstrate that DOT1L affects interneuron development in a cell-autonomous manner. Deletion of Dot1l in MGE-derived interneuron precursor cells results in an overall reduction and altered distribution of GABAergic interneurons in the cortical plate at postnatal day (P) 0. Furthermore, we observed an altered proportion of GABAergic interneurons in the cortex and striatum at P21 with a significant decrease in Parvalbumin (PVALB)-expressing interneurons. Altogether, our results indicate that reduced numbers of cortical interneurons upon DOT1L deletion results from altered postmitotic differentiation/maturation.

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Sprouting transcriptome in cortical neurons

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Gene expression from human iPSC derived cortical neurons

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Neuronal zipcode identification protocol (N-zip) in primary cortical neurons

Project description:For identification of transcripts enriched in neurites of primary cortical neurons, the cells were plated on a microporous membrane for isolation of neurites and soma. Extracted RNA was used for preparation of mRNA-seq, total RNA-seq or smRNA-seq libraries and Illumina sequencing. For neuronal zipcode identification protocol (N-zip) in mouse cortical neurons, we combined a massively parallel reporter assay with neurites/soma separation. Neurons, grown on a microporous membrane, were infected with a library of around 5000 oligos tiled across 3'UTRs of selected neurite-enriched transcripts, cloned downstream of GFP coding sequence. RNA was extracted from soma and neurites and reverse transcribed into cDNA. Amplicon libraries of 3'UTR reporters were prepared and subjected to Illumina sequencing. In the second round of N-zip, a library containing selected reporters from the first N-zip and their mutagenized versions (around 6000 oligos) were used. In the following rounds, N-zip was combined with knockdown of selected genes.

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Transcription profiling of mouse FACS-purified cortical projection neurons

Project description:This SuperSeries is composed of the following subset Series:; GSE2039: FACS purified cortical projection neurons; GSE17783: Analysis of gene expression in FACS-purified cortical projection neurons using Affymetrix 430 2.0 microarrays Experiment Overall Design: Refer to individual Series

2009-10-10 | E-GEOD-17784 | biostudies-arrayexpress

PHF6 knockdown in rat cortical neurons

Project description:E18 embryonic rat cortical neurons cultured in vitro are infected with lentivirus expressing control or PHF6shRNA-2, and harvested 5 days after infection pLL3.7 lentivirus expressing control or PHF6shRNA-2 was generated in 293T cells and concentrated using ultracentrifuge. In vitro cultured cortical neurons were infected and RNA was harvested 5 days after infection. PHF6 knockdown was validated by QPCR before sample was processed for microarray analysis.

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