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Physical interactions between Gsx2 and Ascl1 balance progenitor expansion versus neurogenesis in the mouse lateral ganglionic eminence

ABSTRACT: These findings suggest that physical interactions between Gsx2 and Ascl1 limit Ascl1:Ascl1 and Ascl1:Tcf3 interactions, and thereby inhibit Ascl1-dependennt neurogenesis and allow for progenitor expansion within the LGE.

ORGANISM(S): Mus musculus

PROVIDER: GSE142768 | GEO | 2020/03/11

REPOSITORIES: GEO

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Physical interactions between Gsx2 and Ascl1 balance progenitor expansion versus neurogenesis in the mouse lateral ganglionic eminence

Project description:Physical interactions between Gsx2 and Ascl1 balance progenitor expansion versus neurogenesis in the mouse lateral ganglionic eminence

| PRJNA598224 | ENA

Physical interactions between Gsx2 and Ascl1 balance progenitor expansion versus neurogenesis in the mouse lateral ganglionic eminence.

Project description:The Gsx2 homeodomain transcription factor promotes neural progenitor identity in the lateral ganglionic eminence (LGE), despite upregulating the neurogenic factor Ascl1. How this balance in maturation is maintained is unclear. Here, we show that Gsx2 and Ascl1 are co-expressed in subapical progenitors that have unique transcriptional signatures in LGE ventricular zone (VZ) cells. Moreover, whereas Ascl1 misexpression promotes neurogenesis in dorsal telencephalic progenitors, the co-expression of Gsx2 with Ascl1 inhibits neurogenesis. Using luciferase assays, we found that Gsx2 reduces the ability of Ascl1 to activate gene expression in a dose-dependent and DNA binding-independent manner. Furthermore, Gsx2 physically interacts with the basic helix-loop-helix (bHLH) domain of Ascl1, and DNA-binding assays demonstrated that this interaction interferes with the ability of Ascl1 to bind DNA. Finally, we modified a proximity ligation assay for tissue sections and found that Ascl1-Gsx2 interactions are enriched within LGE VZ progenitors, whereas Ascl1-Tcf3 (E-protein) interactions predominate in the subventricular zone. Thus, Gsx2 contributes to the balance between progenitor maintenance and neurogenesis by physically interacting with Ascl1, interfering with its DNA binding and limiting neurogenesis within LGE progenitors.

| S-EPMC7157596 | biostudies-literature

Bulk RNA-seq of the human fetal neocortex, lateral ganglionic eminence and medial ganglionic eminence at 7, 9, 11 and 20 post-conceptional weeks

Project description:Deep transcriptional profiling of the human neocortex, lateral ganglionic eminence (LGE) and medial ganglionic eminences (MGE), from 7 to 20 post-conceptional weeks (pcw), for de novo lincRNAs discovery and to establish a unique coding and non-coding gene signature for the three different regions.

2021-05-13 | E-MTAB-8893 | biostudies-arrayexpress

Transcriptomic analysis from lateral ganglionic eminence (LGE) of wild type and Gsx2 germline knock-out mice.

Project description:RNA-seq analysis was used to identify genes that are differentially expressed between wild type and Gsx2 null mouse LGEs.

2020-12-04 | GSE162590 | GEO

Transcriptomic analysis from lateral ganglionic eminence (LGE) of wild type and Gsx2 germline knock-out mice.

Project description:Transcriptomic analysis from lateral ganglionic eminence (LGE) of wild type and Gsx2 germline knock-out mice.

| PRJNA682341 | ENA

Single-cell RNA-seq of the human fetal lateral ganglionic eminence at 7, 9 and 11 post-conceptional weeks

Project description:Single-cell RNA-seq of the LGE between 7 and 11 pcw was used to uncover the different cell populations of the developing human striatum and how cells transition from early progenitors to mature medium spiny neuron (MSNs) together with the discovery of their unique coding and non-coding transcriptional signature.

2021-05-13 | E-MTAB-8894 | biostudies-arrayexpress

Characterization of Glcci1 expression in a subpopulation of lateral ganglionic eminence progenitors in the mouse telencephalon.

Project description:BACKGROUND:The lateral ganglionic eminence (LGE) in the ventral telencephalon is a diverse progenitor domain subdivided by distinct gene expression into a dorsal region (dLGE) that gives rise to olfactory bulb and amygdalar interneurons and a ventral region (vLGE) that gives rise to striatal projection neurons. The homeobox gene, Gsx2, is an enriched marker of the LGE and is expressed in a high dorsal to low ventral gradient in the ventricular zone (VZ) as development proceeds. Aside from Gsx2, markers restricted to the VZ in the dLGE and/or vLGE remain largely unknown. RESULTS:Here, we show that the gene and protein expression of Glucocorticoid-induced transcript 1 (Glcci1) has a similar dorsal to ventral gradient of expression in the VZ as Gsx2. We found that Glcci1 gene and protein expression are reduced in Gsx2 mutants, and are increased in the cortex after early and late Gsx2 misexpression. Moreover, Glcci1 expressing cells are restricted to a subpopulation of Gsx2 positive cells on the basal side of the VZ and co-express Ascl1, but not the subventricular zone dLGE marker, Sp8. CONCLUSIONS:These findings suggest that Glcci1 is a new marker of a subpopulation of LGE VZ progenitor cells in the Gsx2 lineage. Developmental Dynamics 247:222-228, 2018. © 2017 Wiley Periodicals, Inc.

| S-EPMC5739986 | biostudies-literature

ChIP-seq on Olig2, Ascl1, Tcf3, Max, NFI, Sox2, Sox9 and Sox21 in mouse neural stem cells

Project description:Definition of genome wide binding profile of Olig2, Ascl1, Tcf3, Max, NFI, Sox2, Sox9 and Sox21 in mouse neural stem cells. Three sets of processed data files, together with a README file (README_E-MTAB-2228.docx) describing the source and content of each file, are provided as additional files to this ArrayExpress submission and can be found in https://www.ebi.ac.uk/arrayexpress/files/E-MTAB-2228 .

2014-09-19 | E-MTAB-2228 | biostudies-arrayexpress

ASCL1: a pioneer factor that induces subtype switching and characterizes adrenergic neuroblastoma

Project description:Neuroblastoma is an embryonic malignancy originating from early nerve cells. Neuroblastoma retains plasticity, interconverting between the mesenchymal (MES) and adrenergic (ADRN) states, which are controlled by different sets of transcription factors forming the core regulatory circuit (CRC). However, their functional roles and cooperative mechanisms in neuroblastoma pathogenesis are poorly understood. Here, we demonstrate that overexpression of ASCL1 in MES neuroblastoma cells opens closed chromatin at the promoters of key ADRN genes, accompanied by epigenetic activation and establishment of enhancer-promoter interactions, thereby initiating subtype switching. ASCL1 inhibits the TGFb-SMAD2/3 pathway but activates the BMP-SMAD1-ID3/4 pathway, serving as negative feedback to balance the function of ASCL1-TCF12 dimers. ASCL1 and other ADRN CRC members potentiate each other’s activity, increasing the expression of the original targets and inducing a new set of genes, thereby promoting conversion to ADRN neuroblastoma. Thus, via its pioneer factor function, ASCL1 serves as a master regulator that characterizes ADRN neuroblastoma.

2023-12-08 | PXD037670 | Pride

The homeobox gene Gsx2 controls the timing of oligodendroglial fate specification in mouse lateral ganglionic eminence progenitors.

Project description:The homeobox gene Gsx2 has previously been shown to be required for the specification of distinct neuronal subtypes derived from lateral ganglionic eminence (LGE) progenitors at specific embryonic time points. However, its role in the subsequent generation of oligodendrocytes from these progenitors remains unclear. We have utilized conditional gain-of-function and loss-of-function approaches in order to elucidate the role of Gsx2 in the switch between neurogenesis and oligodendrogenesis within the embryonic ventral telencephalon. In the absence of Gsx2 expression, an increase in oligodendrocyte precursor cells (OPCs) with a concomitant decrease in neurogenesis is observed in the subventricular zone of the LGE at mid-stages of embryogenesis (i.e. E12.5-15.5), which subsequently leads to an increased number of Gsx2-derived OPCs within the adjacent mantle regions of the cortex before birth at E18.5. Moreover, using Olig2(cre) to conditionally inactivate Gsx2 throughout the ventral telencephalon with the exception of the dorsal (d)LGE, we found that the increase in cortical OPCs in Gsx2 germline mutants are derived from dLGE progenitors. We also show that Ascl1 is required for the expansion of these dLGE-derived OPCs in the cortex of Gsx2 mutants. Complementing these results, gain-of-function experiments in which Gsx2 was expressed throughout most of the late-stage embryonic telencephalon (i.e. E15.5-18.5) result in a significant decrease in the number of cortical OPCs. These results support the notion that high levels of Gsx2 suppress OPC specification in dLGE progenitors and that its downregulation is required for the transition from neurogenesis to oligodendrogenesis.

| S-EPMC3653554 | biostudies-literature

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