Transcription factor 4 controls positioning of cortical projection neurons through regulation of cell adhesion
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ABSTRACT:
PROVIDER: PRJNA700842 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13665060_1.fastq.gz | Fastqsanger.gz | |||
| SRR13665060_2.fastq.gz | Fastqsanger.gz | |||
| SRR13665061_1.fastq.gz | Fastqsanger.gz | |||
| SRR13665061_2.fastq.gz | Fastqsanger.gz | |||
| SRR13665062_1.fastq.gz | Fastqsanger.gz |
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Project description:The establishment of neural circuits depends on precise neuronal positioning in the cortex, a tightly coordinated process of neuronal differentiation, migration and terminal localization. Deficit in this process is implicated in several psychiatric disorders. Here, we show that the transcription factor Tcf4 controls neuronal positioning during brain development. Tcf4-deficient neurons become mispositioned in clusters when their migration to the cortical plate is complete. We reveal that Tcf4 regulates the expression of cell adhesion molecules to control neuronal positioning. Furthermore, through in vivo extracellular electrophysiology, we show that neuronal functions are disrupted after the loss of Tcf4. TCF4 mutations are strongly associated with schizophrenia and cause Pitt-Hopkins syndrome, which is characterized by severe intellectual disability. Thus, our results not only reveal the importance of neuronal positioning in brain development and but also provide new insights into the potential mechanisms underlying neurological defects linked to TCF4 mutations.
2021-09-20 | GSE166412 | GEO
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
Project description:3 subtypes of cortical projection neurons were purified by fluorescence-activated cell sorting at 4 different stages of development from mouse cortex. A detailed description of the data set is described in Arlotta, P et al (2005)
2007-11-20 | E-GEOD-2039 | biostudies-arrayexpress
Project description:3 subtypes of cortical projection neurons were purified by fluorescence-activated cell sorting at 4 different stages of development from mouse cortex. A detailed description of the data set is described in Arlotta, P et al (2005). Keywords = corticospinal motor neuron callosal corticotectal cortex development FACS
2005-01-19 | GSE2039 | GEO
Project description:3 subtypes of cortical projection neurons were purified by fluorescence-activated cell sorting (FACS) at 4 different stages of development from mouse cortex. A detailed description of the data set is described in Arlotta, P et al (2005) and Molyneaux, BJ et al (2009). The hybridization cocktails used here were originally applied to the Affymetrix mouse 430A arrays and submitted as GEO accession number GSE2039. The same hybridization cocktails were then applied to the Affymetrix mouse 430 2.0 arrays, and those data are contained in this series. Experiment Overall Design: Three subtypes of cortical neurons were purified by FACS at multiple stages of mouse brain development. The neuron subtypes are: corticospinal motor neurons (CSMN), callosal projection neurons (CPN), and corticotectal projection neurons (CTPN). The stages of development included embryonic day 18 (E18), postnatal day 3 (P3), postnatal day 6 (P6), and postnatal day 14 (P14). CSMN and CPN were analyzed at all four stages, while CTPN were only analyzed at P14. The replicates included in the data set are all true biological replicates with independent sample collection for each.
2009-10-09 | E-GEOD-17783 | biostudies-arrayexpress
Project description:Neuronal cell types are classically defined by their molecular properties, anatomy, and functions. While recent advances in single-cell genomics have led to high-resolution molecular characterization of cell type diversity in the brain, neuronal cell types are often studied out of the context of their anatomical properties. To better understand the relationship between molecular and anatomical features defining cortical neurons, we developed Epi-Retro-Seq, a method that combined retrograde labeling with single-nucleus DNA methylation sequencing to link epigenomic properties of cell types to neuronal projections. We profiled 16,971 single neocortical neurons from 63 cortico-cortical and cortico-subcortical long-distance projections. Our results revealed unique epigenetic signatures of projection neurons that correspond to their laminar and regional location and projection patterns. The methylomes of 16,971 mouse neocortical neurons from 63 cortico-cortical (CC) and cortico-subcortical long-distance projections were analyzed using Epi-Retro-Seq, a method that combined retrograde tracing and single nucleus methylome sequencing.
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Project description:In the cerebral cortex, projection neurons and interneurons work coordinately to establish functional neural networks and to control the balance between excitatory versus inhibitory synaptic activities for normal cortical functions. While the specific mechanisms that control productions of projection neurons and interneurons are beginning to be revealed, a global characterization of the molecular differences between these two groups of neurons is in need for a more comprehensive understanding of their developmental specifications as well as their cortical functions. Previous studies have shown that the majority of cortical projection neurons are produced by radial glial cells (RGCs) through intermediate progenitor cells (IPCs) which can be marked by the expression of transcription factor Tbr2(Eomes). In this study, taking advantage of lineage tracing power of combining Tbr2(Eomes)-GFP and DCX-mRFP transgenic reporter mice, we prospectively separated IPC-derived neurons (IPNs) from non-IPC-derived neurons (non-IPNs) of the embryonic cortex. Molecular characterizations revealed that IPNs and non-IPNs were enriched with projection neurons and interneurons, respectively. Transcriptome analyses documented distinct groups of genes differentially expressed between these two groups of neurons. These data present a useful resource for further investigation of the molecular regulations and functions of projection neurons and interneurons.
2015-08-12 | GSE62042 | GEO
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.
2022-06-24 | GSE185288 | GEO
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.
2022-06-24 | GSE185287 | GEO
Project description:Completion of neuronal migration is critical for brain development. Kif21b is a plus-end directed kinesin motor protein that promotes intracellular transport and controls microtubule dynamics in neurons. Here we report a physiological function of Kif21b during radial migration of projection neurons in the mouse developing cortex. In vivo analysis in mouse and live imaging on cultured slices demonstrate that Kif21b regulates the radial glia-guided locomotion of new-born neurons independently of its motility on microtubules. Unexpectedly we show that Kif21b directly binds and regulates the actin cytoskeleton both in vitro and in vivo in migratory neurons. We establish that Kif21b-mediated regulation of actin cytoskeleton dynamics influences branching and nucleokinesis during neuronal locomotion. Altogether, our results reveal atypical roles of Kif21b on the actin cytoskeleton during migration of cortical projection neurons
2023-07-04 | PXD042855 | Pride