Mus musculus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR186622.fastq.gz | Fastqsanger.gz | |||
| DRR186623.fastq.gz | Fastqsanger.gz | |||
| DRR186624.fastq.gz | Fastqsanger.gz | |||
| DRR186625.fastq.gz | Fastqsanger.gz | |||
| DRR186626.fastq.gz | Fastqsanger.gz |
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Project description:The mechanisms by which Hmga2 regulates neurogenic potential of embryonic and neocortical neural precursor cells
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Project description:Neural precursor cells (NPCs) in the mammalian neocortex generate various neuronal and glial cell types in a developmental stage-dependent manner. Most neocortical NPCs lose their neurogenic potential after birth. We have previously shown that high mobility group A (HMGA) proteins confer the neurogenic potential on early-stage NPCs during the midgestation period, although the underlying mechanisms are not fully understood. Here we performed microarray analysis and compared expression profiles between control and HMGA2-overexpressed NPCs. Mouse neocortical neuroepithelial cells were isolated at embryonic day 11.5 and cultured as neurospheres for 9 days in vitro in the presence of fibroblast growth factor (FGF) 2 and epidermal growth factor (EGF). These cells were infected with control or HMGA2-expressing retrovirus, cultured in the presence of FGF and EGF for 3 days. Half of them were collected immediately for microarray analysis, and the other half were cultured in the absence of FGF for 12 h and then collected for microarray analysis.
2013-02-01 | E-GEOD-41882 | biostudies-arrayexpress
Project description:Neural precursor cells (NPCs) in the mammalian neocortex generate various neuronal and glial cell types in a developmental stage-dependent manner. Most neocortical NPCs lose their neurogenic potential after birth. We have previously shown that high mobility group A (HMGA) proteins confer the neurogenic potential on early-stage NPCs during the midgestation period, although the underlying mechanisms are not fully understood. Here we performed microarray analysis and compared expression profiles between control and HMGA2-overexpressed NPCs.
2013-02-01 | GSE41882 | GEO
Project description:We demonstrate for the first time that the extracellular matrix glycoprotein Tenascin-C regulates the expression of key patterning genes during late embryonic spinal cord development, leading to a timely maturation of gliogenic neural precursor cells. We first show that Tenascin-C is expressed by gliogenic neural precursor cells during late embryonic development. The loss of Tenascin-C leads to a sustained generation and delayed migration of Fibroblast growth factor receptor 3 expressing immature astrocytes in vivo. Furthermore, we could demonstrate an upregulation of Nk2 transcription factor related locus 2 (Nkx2.2) and its downstream target Sulfatase 1 in vivo. A dorsal expansion of Nkx2.2-positive cells within the ventral spinal cord indicates a potential progenitor cell domain shift. Moreover, Sulfatase 1 is known to regulate growth factor signalling by cleaving sulphate residues from heparan sulphate proteoglycans. Consistent with this possibility we observed changes in both Fibroblast growth factor 2 and Epidermal growth factor responsiveness of spinal cord neural precursor cells. Taken together our data clearly show that Tenascin-C promotes the astroglial lineage progression during spinal cord development. in total 6 probes: 3 replica of TNC_wt and 3 replica of TNC_ko
2011-10-19 | E-GEOD-33091 | biostudies-arrayexpress
Project description:During development, the meninges act as a regulator of neocortical development by secreting ligands that act on neural cells to regulate neurogenesis and neuronal migration. Meninges-derived retinoic acid (RA) promotes neocortical progenitor cell cycle exit however the underlying mechanism is unknown. Here, we use Foxc1-mutant embryos that lack meninges-derived ligands, spatial transcriptomics, and profiling of retinoic-acid receptor-a (RARa) DNA binding to identify the neurogenic transcriptional mechanisms of RA signaling in cortical neural progenitors. We determined that meningeal-derived RA controls neurogenesis by suppressing self-renewal pathways Notch signaling and the transcription factor Sox2. We show that RARα binds in the Sox2ot promoter, a long non-coding RNA that regulates Sox2 expression, and RA promotes Sox2ot expression in neocortical progenitors. Our findings elucidate a previously unknown mechanism of howmeningeal RA coordinates neocortical development and insight into how defects in meningeal develop can cause neurodevelopmental disorders.
2024-09-25 | GSE269283 | GEO
Project description:During development, the meninges act as a regulator of neocortical development by secreting ligands that act on neural cells to regulate neurogenesis and neuronal migration. Meninges-derived retinoic acid (RA) promotes neocortical progenitor cell cycle exit however the underlying mechanism is unknown. Here, we use Foxc1-mutant embryos that lack meninges-derived ligands, spatial transcriptomics, and profiling of retinoic-acid receptor-a (RARa) DNA binding to identify the neurogenic transcriptional mechanisms of RA signaling in cortical neural progenitors. We determined that meningeal-derived RA controls neurogenesis by suppressing self-renewal pathways Notch signaling and the transcription factor Sox2. We show that RARα binds in the Sox2ot promoter, a long non-coding RNA that regulates Sox2 expression, and RA promotes Sox2ot expression in neocortical progenitors. Our findings elucidate a previously unknown mechanism of howmeningeal RA coordinates neocortical development and insight into how defects in meningeal develop can cause neurodevelopmental disorders.
2024-09-25 | GSE269282 | GEO
Project description:We demonstrate for the first time that the extracellular matrix glycoprotein Tenascin-C regulates the expression of key patterning genes during late embryonic spinal cord development, leading to a timely maturation of gliogenic neural precursor cells. We first show that Tenascin-C is expressed by gliogenic neural precursor cells during late embryonic development. The loss of Tenascin-C leads to a sustained generation and delayed migration of Fibroblast growth factor receptor 3 expressing immature astrocytes in vivo. Furthermore, we could demonstrate an upregulation of Nk2 transcription factor related locus 2 (Nkx2.2) and its downstream target Sulfatase 1 in vivo. A dorsal expansion of Nkx2.2-positive cells within the ventral spinal cord indicates a potential progenitor cell domain shift. Moreover, Sulfatase 1 is known to regulate growth factor signalling by cleaving sulphate residues from heparan sulphate proteoglycans. Consistent with this possibility we observed changes in both Fibroblast growth factor 2 and Epidermal growth factor responsiveness of spinal cord neural precursor cells. Taken together our data clearly show that Tenascin-C promotes the astroglial lineage progression during spinal cord development.
2011-10-20 | GSE33091 | GEO
Project description:Neocortical projection neurons of mammalian brains are largely direct daughters of intermediate progenitors (IP), which are progenies of radial glial cells (RG). The maintenance of the RG pool, production and expansion of IPs are essential for neocortical formation during development, as well as neocortical expansion during evolution. Here we characterized an epigenetic circuit that controls precise neurogenic programming of the neocortex. The circuit comprises a long non-coding RNA – LncBAR and the SWI/SNF (BAF) chromatin-remodeling complex, which transcriptionally maintains the expression of Zbtb20. LncBAR knockout neocortex contains fewer upper-layer projection neurons. Intriguingly, loss of LncBAR promotes IP production of RGCs, but hampers neurogenic division and lengthens the cell-cycle durations of IPs during mid-later cortical neurogenesis. Moreover, in LncBAR knockout mice, depletion of the neural progenitor pool at embryonic stage causes fewer adult neural stem cells at the subventricular zone, leading to compromised adult neurogenesis to replenish the olfactory bulb. LncBAR binds to BRG1, the core enzymatic component of the SWI/SNF (BAF) chromatin-remodeling complex. LncBAR depletion enhances association of BRG1 with and the genomic locus of, and suppresses the expression of Zbtb20, a transcription factor gene known to regulate both embryonic and adult neurogenesis. ZBTB20 re-expression in LncBAR-knockout neural precursors reversed compromised neurogenic divisions of IPCs. Together, we revealed a previously unidentified epigenetic machinery to control neurogenesis of neural precursors.
2021-10-27 | GSE169164 | GEO
Project description:Neocortical projection neurons of mammalian brains are largely direct daughters of intermediate progenitors (IP), which are progenies of radial glial cells (RG). The maintenance of the RG pool, production and expansion of IPs are essential for neocortical formation during development, as well as neocortical expansion during evolution. Here we characterized an epigenetic circuit that controls precise neurogenic programming of the neocortex. The circuit comprises a long non-coding RNA – LncBAR and the SWI/SNF (BAF) chromatin-remodeling complex, which transcriptionally maintains the expression of Zbtb20. LncBAR knockout neocortex contains fewer upper-layer projection neurons. Intriguingly, loss of LncBAR promotes IP production of RGCs, but hampers neurogenic division and lengthens the cell-cycle durations of IPs during mid-later cortical neurogenesis. Moreover, in LncBAR knockout mice, depletion of the neural progenitor pool at embryonic stage causes fewer adult neural stem cells at the subventricular zone, leading to compromised adult neurogenesis to replenish the olfactory bulb. LncBAR binds to BRG1, the core enzymatic component of the SWI/SNF (BAF) chromatin-remodeling complex. LncBAR depletion enhances association of BRG1 with and the genomic locus of, and suppresses the expression of Zbtb20, a transcription factor gene known to regulate both embryonic and adult neurogenesis. ZBTB20 re-expression in LncBAR-knockout neural precursors reversed compromised neurogenic divisions of IPCs. Together, we revealed a previously unidentified epigenetic machinery to control neurogenesis of neural precursors.
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Project description:Transcriptomic, epigenetic and chromatin changes of the embryonic and neocortical neural precursor cells in the stage dependent manner
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