Mus musculus strain:Swiss | isolate:embryonic mouse brain cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA886320 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21798508_1.fastq.gz | Fastqsanger.gz | |||
| SRR21798508_2.fastq.gz | Fastqsanger.gz | |||
| SRR21798509_1.fastq.gz | Fastqsanger.gz | |||
| SRR21798509_2.fastq.gz | Fastqsanger.gz | |||
| SRR21798510_1.fastq.gz | Fastqsanger.gz |
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Project description:Extracellular matrix-inducing Sox9 orchestrates basal progenitor proliferation and gliogenesis in developing neocortex
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Project description:Activation of Map kinase/Erk signalling downstream of fibroblast growth factor (Fgf) tyrosine kinase receptors regulates gene expression required for mesoderm induction and patterning of the anteroposterior axis during Xenopus development. We have proposed that a subset of Fgf target genes are activated in the embyo in response to inhibition of a transcriptional repressor. Here we investigate the hypothesis that Cic (Capicua), which was originally identified as a transcriptional repressor negatively regulated by receptor tyrosine kinase/Erk signalling in Drosophila, is involved in regulating Fgf target gene expression in Xenopus. We characterise Xenopus Cic and show that it is widely expressed in the embryo. Fgf overexpression or ectodermal wounding, both of which potently activate Erk, reduce Cic protein levels in embryonic cells. A similar mechanism of Cic protein degradation downstream of the Torso receptor tyrosine kinase receptor negatively regulates Cic activity in Drosophila. In keeping with our hypothesis, we show that Cic knockdown and Fgf overexpression have overlapping effects on embryo development and gene expression. Transcriptomic analysis identifies a cohort of genes that are up-regulated by Fgf overexpression and Cic knockdown. We investigate two of these genes, fos and rasl11b, which, respectively, encode a leucine zipper transcription factor and a ras family GTPase, as putative targets of the proposed Fgf/Erk/Cic axis. We identify Cic consensus binding sites in a highly conserved region of intron 1 in the fos gene and Cic sites in the upstream regions of several other Fgf/Cic co-regulated genes, including rasl11b. We show that expression of fos and rasl11b is blocked in the early mesoderm when Fgf and Erk signalling is inhibited. In addition, we show that fos and rasl11b expression is associated with the Fgf independent activation of Erk at the site of ectodermal wounding. Our data support a role for a Fgf/Erk/Cic axis in regulating a subset of Fgf target genes during gastrulation and is suggestive that Erk signalling is involved in regulating Cic target genes at the site of ectodermal wounding.
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Project description:Neocortex expansion is largely based on the proliferative capacity of basal progenitors (BPs), which is increased by extracellular matrix (ECM) components via integrin signaling. Here we show that Sox9 drives expression of ECM components and that laminin 211 increases BP proliferation in embryonic mouse neocortex. Examination of Sox9 expression reveals that Sox9 is expressed in BPs of developing ferret and human, but not mouse neocortex. Functional studies by conditional Sox9 expression in the mouse BP lineage demonstrate increased BP proliferation, reduced Tbr2 and induction of Olig2 expression, indicative of premature gliogenesis. Conditional Sox9 expression also results in cell non-autonomous stimulation of BP proliferation followed by increased production of upper-layer neurons. Collectively, our findings demonstrate that Sox9 exerts concerted effects on transcription, BP proliferation, neuron production, and neurogenic as well as gliogenic BP cell fate, suggesting that Sox9 acts a master regulator in the subventricular zone to promote neocortical expansion.
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Project description:In this experiment we inhibited FGF signalling in E14.5 mouse lungs by using a dominant negative mouse model. We are interested in assessing the genetic regulation by FGF signalling at this stage of lung development. Specifically, we used a tetracycline controlled transcriptional activation model (Tet(o)) to manipulate FGF signalling. Genetically modified male mice that expressed a reverse tetracycline-controlled trans activator (rtTA) on the Rosa26 locus and a soluble FGFR2b on the Tet(o) promoter (Tet(o)sFgfr2b) (B6.Cg-Gt(ROSA)26Sortm1.1(rtTA,EGFP)NagyTg(tetO-Fgfr2b/Igh)1.3Jaw/sbel), were crossed with females lacking the Tet(o)sFgfr2b allele. Pregnant females were injected with doxycycline intraperitonally at E14.5. Doxycycline then induced the transcription soluble FGFR2b in the embryos, which inhibited FGF signalling by sequestering FGF ligands, preventing them from binding to the native FGFR2b receptor. We harvested embryonic lungs after 9 hrs of inhibition. We took the left lobe of each sample for RNA isolation. We set-up our matings so that 50% of the embryos in a litter were expected to contain the soluble FGFR2b. The remaining littermates will serve as the control group. We will compare the gene expression profiles of the experimental embryonic lungs with those of littermate controls.
2020-06-22 | GSE115876 | GEO
Project description:In this experiment we inhibited FGF signalling in E16.5 mouse lungs by using a dominant negative mouse model. We are interested in assessing the genetic regulation by FGF signalling at this stage of lung development. Specifically, we used a tetracycline controlled transcriptional activation model (Tet(o)) to manipulate FGF signalling. Genetically modified male mice that expressed a reverse tetracycline-controlled trans activator (rtTA) on the Rosa26 locus and a soluble FGFR2b on the Tet(o) promoter (Tet(o)sFgfr2b) (B6.Cg-Gt(ROSA)26Sortm1.1(rtTA,EGFP)NagyTg(tetO-Fgfr2b/Igh)1.3Jaw/sbel), were crossed with females lacking the Tet(o)sFgfr2b allele. Pregnant females were injected with doxycycline intraperitonally at E16.5. Doxycycline then induced the transcription soluble FGFR2b in the embryos, which inhibited FGF signalling by sequestering FGF ligands, preventing them from binding to the native FGFR2b receptor. We harvested embryonic lungs after 9 hrs of inhibition. We took the left lobe of each sample for RNA isolation. We set-up our matings so that 50% of the embryos in a litter were expected to contain the soluble FGFR2b. The remaining littermates will serve as the control group. We will compare the gene expression profiles of the experimental embryonic lungs with those of littermate controls.
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Project description:A specific subpopulation of neural progenitor cells, the basal radial glia cells (bRGCs) of the outer subventricular zone (OSVZ), are thought to have a key role in the evolutionary expansion of mammalian neocortex. In the developing lissencephalic mouse neocortex, bRGCs exist at low abundance and show significant molecular differences from bRGCs in developing gyrencephalic species. Here, we demonstrate that developing mouse medial neocortex, in contrast to the canonically studied lateral neocortex, exhibits an OSVZ and an abundance of bRGCs similar to that in developing gyrencephalic neocortex. Unlike bRGCs in developing mouse lateral neocortex, the bRGCs in medial neocortex exhibit human bRGC-like gene expression, including expression of Hopx, a human bRGC marker. Disruption of Hopx expression in mouse embryonic medial neocortex and forced Hopx expression in mouse embryonic lateral neocortex demonstrate that Hopx is required and sufficient, respectively, for a bRGC abundance as found in developing gyrencephalic neocortex. Taken together, our data identify a novel bRGC subpopulation in developing mouse medial neocortex that is highly related to bRGCs of developing gyrencephalic neocortex.
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Project description:Gene expression microarray analysis of hESCs treated with BMP4 in chemically-defined medium, with and without inhibitors of Activin and FGF signalling (which maintain pluripotency), to investigate the induction of extra-embryonic tissue (trophectoderm) differentiation by BMP signalling.
2009-07-31 | E-MEXP-1192 | biostudies-arrayexpress
Project description:The forkhead transcription factor FoxO6 is prominently expressed during development of the murine neocortex. However, its function in cortical development is as yet unknown. We now demonstrate that cortical development is altered in FoxO6+/- and FoxO6-/- mice, showing migrating neurons halted in the intermediate zone. Using a FoxO6-directed siRNA approach, we substantiate the requirement of FoxO6 for a correct radial migration in the developing neocortex. Subsequent genome-wide transcriptome analysis reveals altered expression of genes involved in cell adhesion, axon guidance, and gliogenesis upon silencing of FoxO6 We then show that FoxO6 binds to DAF-16-binding elements in the Plexin A4 (Plxna4) promoter region and affects Plxna4 expression. Finally, ectopic Plxna4 expression restores radial migration in FoxO6+/- and siRNA-mediated knockdown models. In conclusion, the presented data provide insights into the molecular mechanisms whereby transcriptional programs drive cortical development.
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