Ascl1 ChIP-seq experiment from ventral telencephalon at E14.5 embryos.
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB41229 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4822760.fastq.gz | Fastqsanger.gz | |||
| ERR4822761.fastq.gz | Fastqsanger.gz | |||
| ERR4822762.fastq.gz | Fastqsanger.gz | |||
| ERR4822763.fastq.gz | Fastqsanger.gz | |||
| ERR4822764.fastq.gz | Fastqsanger.gz |
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Project description:Here we performed a ChIP-seq experiment on a sample of ventral telencephalon from E14.5 embryos. This resulted in the generation of a genome-wide map of Ascl1 binding to chromatin.
2021-07-03 | E-MTAB-9751 | biostudies-arrayexpress
Project description:TESS_E14.5_Adult series: Set of microarray expreriments used to identify genes of TESS library preferentially expressed in Embryonic E14.5 mouse telencephalon Keywords: other
2004-07-31 | GSE1598 | GEO
Project description:The homeobox containing gene Arx is expressed during ventral telencephalon development and it is required for correct GABAergic interneuron tangential migration from the ganglionic eminences to the olfactory bulbs, cerebral cortex and striatum. Its human ortholog is associated with a variety of neurological clinical manifestations whose syntoms are compatible with a loss of cortical interneurons and altered basal ganglia related-activities in humans. Herein, we reported the identification by global expression profiling of a group of genes whose expression is consistently altered in Arx mutant ganglionic eminences. Following analysis revealed the striking ectopic expression in the ganglionic eminences of a number of genes normally not, or only marginally, expressed in the ventral telencephalon. Among them, we functionally analyzed Ebf3, whose ectopic expression in ventral telencephalon is preventingneuronal tangential migration. Further, we showed that Arx is sufficient to repress Ebf3 endogenous expression and that its silencing in Arx mutant tissue might marginally rescue tangential cell movements. Together, these data provide an initial analysis of the molecular pathways regulated by Arx and how their networking might regulate those specific cellular processes during telencephalon development strongly altered by loss of Arx. Three timed-pregnant Arx heterozygous dams crossed with C57Bl/6 males were sacrificed at E14.5, the embryos harvested and placed into cold PBS. After brain isolarion, meninges and olfactory bulbs were removed, and the ventral telencephalon separated from the overlying cerebral cortex. The same procedure was repeated for 5 wt and 5 Arx mutant embryos.
2010-03-09 | E-GEOD-12956 | biostudies-arrayexpress
Project description:As a proneural gene, ASCL1 was reported to be important to neurogenesis. To better illustrate the role of ASCL1 in human telencephalon development, we genetically engineered an ASCL1 knockout (KO) hESC line and ASCL1 rescue (RE) hESC line, and then preformed RNA sequencing when WT, KO and RE were differentiated into neural progenitors in vitro. Our results showed that ASCL1 KO hESCs could be regularly maintained in vitro, and could be efficiently specified into neuroectoderm cells and following telencephalic neural progenitors. Remarkably, dorsal progenitors-derived from ASCL1 KO hESCs failed to differentiate into DCX positive neuroblasts. In addition, dorsal and ventral progenitors retained higher expression of VZ/ESVZ genes but had much lower expression of LSVZ genes after KO of ASCL1. Re-introducing of ASCL1 in KO hESCs through a doxycycline (Dox) inducible overexpression system reversed the gene expression changes induced by cortical progenitors with ASCL1 KO. Taken all these together, our results revealed a pivotal role of ASCL1 in both dorsal and ventral telencephalic development by progressing the cycling progenitors within the ESVZ to post-mitotic early born neurons in the LSVZ in human telencephalon.
2022-12-21 | GSE149096 | GEO
Project description:The homeobox containing gene Arx is expressed during ventral telencephalon development and it is required for correct GABAergic interneuron tangential migration from the ganglionic eminences to the olfactory bulbs, cerebral cortex and striatum. Its human ortholog is associated with a variety of neurological clinical manifestations whose syntoms are compatible with a loss of cortical interneurons and altered basal ganglia related-activities in humans. Herein, we reported the identification by global expression profiling of a group of genes whose expression is consistently altered in Arx mutant ganglionic eminences. Following analysis revealed the striking ectopic expression in the ganglionic eminences of a number of genes normally not, or only marginally, expressed in the ventral telencephalon. Among them, we functionally analyzed Ebf3, whose ectopic expression in ventral telencephalon is preventingneuronal tangential migration. Further, we showed that Arx is sufficient to repress Ebf3 endogenous expression and that its silencing in Arx mutant tissue might marginally rescue tangential cell movements. Together, these data provide an initial analysis of the molecular pathways regulated by Arx and how their networking might regulate those specific cellular processes during telencephalon development strongly altered by loss of Arx.
2010-02-26 | GSE12956 | GEO
Project description:To elucidate whether or not a subtype of adenocarcinoma with neuroendocrine nature has poor prognosis, we performed gene expression profiling of an achaete-scute complex homolog 1 (ASCL1) siRNA experiment. siRNA againt ASCL1 was transfected into DMS79 cells.
2011-07-18 | E-GEOD-21216 | biostudies-arrayexpress
Project description:Heterogeneous astrocyte populations are defined by diversity in cellular environment, progenitor identity or function. Yet, little is known about the extent of the heterogeneity and how this diversity is acquired during development. We used SILAC and quantitative proteomics to characterise primary murine telencephalic progenitor cells from FOXG1 (forkhead box G1)-cre driven Tgfbr2 (transforming growth factor beta receptor 2) knockout mice and identified differential protein expression of the astrocyte proteins GFAP (glial fibrillary acidic protein) and MFGE8 (milk fat globule-EGF factor 8). Biochemical and histological investigations revealed distinct populations of astrocytes in the dorsal and ventral telencephalon marked by GFAP or MFGE8 protein expression. The two subtypes differed in their response to TGFβ-signalling. Impaired TGFβ-signalling affected numbers of GFAP-astrocytes in the ventral telencephalon. In contrast, TGFβ reduced MFGE8 expression in astrocytes deriving from both regions. Additionally, lineage tracing revealed that both GFAP and MFGE8 astrocyte subtypes derived partly from FOXG1-expressing neural precursor cells.
2022-03-02 | PXD005072 | Pride
Project description:In rodent ventral telencephalon, diffusible morphogens induce expression of the proneural transcription factor ASCL1, which in turn induces expression of the transcription factor DLX2 that controls differentiation of cortical interneuron precursors and their tangential migration to the cerebral cortex. RNAseq analysis of human fetal samples of dorsal telencephalon revealed consistently high cortical expression of ASCL1 and increasing expression of DLX2 between 7.5 and 17 post-conceptional weeks (PCW). We explored whether cortical expression of these genes represented a population of intracortically derived interneuron precursors. Immunohistochemistry revealed an ASCL1+ /DLX2+ population of progenitor cells in the human ganglionic eminences between 6.5 and 12 PCW, but in the cortex there also existed a population of ASCL1+ /DLX2- progenitors in the subventricular zone (SVZ) that largely co-expressed cortical markers PAX6 or TBR2, although a few ASCL1+ /PAX6- progenitors were observed in the ventricular zone (VZ) and ASCL1+ cells expressing the interneuron marker GAD67 were present in the SVZ. Although rare in the VZ, DLX2+ cells progressively increased in number between 8 and 12 PCW across the cortical wall and the majority co-expressed LHX6 and originated either in the MGE, migrating to the lateral cortex, or from the septum, populating the medial wall. A minority co-expressed COUP-TFII, which identifies cells from the caudal ganglionic eminence (CGE). By 19 PCW, a significant increase in expression of DLX2 and ASCL1 was observed in the cortical VZ with a small proportion expressing both proteins. The DLX2+ cells did not co-express a cell division marker, so were not progenitors. The majority of DLX2+ cells throughout the cortical plate expressed COUP-TFII rather than LHX6+ . As the VZ declined as a proliferative zone it appeared to be re-defined as a migration pathway for COUP-TFII+ /DLX2+ interneurons from CGE to cortex. Therefore, in developing human cortex, ASCL1 expression predominantly marks a population of intermediate progenitors giving rise to glutamatergic neurons. DLX2 expression predominantly defines post-mitotic interneuron precursors.
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Project description:Tamoxifen was administered to Glast-CreER;Nf1-flox/flox;Tp53-flox/flox or Glast-CreER;Ascl1-flox/flox;Nf1-flox/flox;Tp53-flox/flox at E14.5 to induce tumors in the brain
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