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Nkx2.2, Nkx6.1, Olig2, and Gli3 genomic binding regions and overexpression in neural progenitors

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE65462 | GEO | 2015/08/24

SECONDARY ACCESSION(S): PRJNA274056

REPOSITORIES: GEO

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Nkx2.2, Nkx6.1, Olig2, and Gli3 genomic binding regions and overexpression in neural progenitors

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-08-24 | E-GEOD-65462 | biostudies-arrayexpress

Nkx2.2, Nkx6.1, Olig2, and Gli3 genomic binding regions in neural progenitors [ChIP-Seq]

Project description:Nkx2.2, Nkx6.1, and Olig2 are transcriptional repressors regulating somatic motor neuron and interneuron subtypes in neural progenitors. The purpose of this study was to identify their target genes and to elucidate their gene regulatory mechanisms, including their relationship to Sonic Hedgehog/Gli pathway.

2015-08-24 | GSE61673 | GEO

mRNAseq analysis of Nkx2.2, Nkx6.1, and Olig2 overexpression in neural progenitors

Project description:Nkx2.2, Nkx6.1, and Olig2 repressors were overexpressed, singly or in combination, in in vitro-derived mouse neural progenitors to identify thier repression targets

2015-08-24 | GSE65457 | GEO

mRNAseq analysis of Nkx2.2, Nkx6.1, and Olig2 overexpression in neural progenitors

Project description:Nkx2.2, Nkx6.1, and Olig2 repressors were overexpressed, singly or in combination, in in vitro-derived mouse neural progenitors to identify thier repression targets Overexpression study to identify genes repressed by Nkx2.2, Nkx6.1, and Olig2 in neural progenitors

2015-08-24 | E-GEOD-65457 | biostudies-arrayexpress

Phosphorylation state of Olig2 regulates proliferation of neural progenitors.

Project description:The bHLH transcription factors that regulate early development of the central nervous system can generally be classified as either antineural or proneural. Initial expression of antineural factors prevents cell cycle exit and thereby expands the pool of neural progenitors. Subsequent (and typically transient) expression of proneural factors promotes cell cycle exit, subtype specification, and differentiation. Against this backdrop, the bHLH transcription factor Olig2 in the oligodendrocyte lineage is unorthodox, showing antineural functions in multipotent CNS progenitor cells but also sustained expression and proneural functions in the formation of oligodendrocytes. We show here that the proliferative function of Olig2 is controlled by developmentally regulated phosphorylation of a conserved triple serine motif within the amino-terminal domain. In the phosphorylated state, Olig2 maintains antineural (i.e., promitotic) functions that are reflected in human glioma cells and in a genetically defined murine model of primary glioma.

| S-EPMC3065213 | biostudies-literature

OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors.

Project description:Mental retardation and early Alzheimer's disease (AD) have generally been attributed to progressive neuronal loss in the developing and mature Down syndrome (DS) brain. However, reduced neuronal production during development could also contribute to the smaller brain size and simplified gyral patterning seen in this disorder. Here, we show impairments in proliferation within the ventricular zone (VZ) of early DS fetal cortex and in cultured early passage DS human neural progenitors (HNPs). We find that the reduced proliferative rates correspond temporally with increased expression of the chromosome 21 (HSA21) associated, oligodendrocyte transcription factor OLIG2 at 14-18 weeks gestational age (GA) (period of neurogenesis). Moreover, the DS HNPs adopt more oligodendrocyte-specific features including increased oligodendrocyte marker expression, as well as a reduction in KCNA3 potassium channel expression and function. We further show that OLIG2 inhibition or over-expression regulates potassium channel expression levels and that activation or inhibition of these channels influences the rate of progenitor proliferation. Finally, neural progenitors from Olig2 over-expressing transgenic mice exhibit these same impairments in proliferation and potassium channel expression. These findings suggest that OLIG2 over-expression inhibits neural progenitor proliferation through changes in potassium channel activity, thereby contributing to the reduced neuronal numbers and brain size in DS.

| S-EPMC3335315 | biostudies-literature

GLI3 binding regions in mouse embryonic forelimb buds

Project description:Purpose: The response to Hedgehog signaling in the limb is driven by GLI bound enhancers and the majority of Hh targets in the developing limb bud are regulated solely by the activity of GLI-repressor. Currently we do not have a comprehensive understanding of how GLI bound enhancers respond Hedgehog signaling. The goal of this study is to identify how GLI bound enhancers are regulated by Hedgehog signaling and specifically by GLI-repressor. Methods: ChIP-seq was performed in Embryonic day 10.5 mouse limb buds from mice with endogenously FLAG tagged Gli3. Results: We identified 7282 GLI3 binding regions in the E10.5 limb bud.

2020-01-21 | GSE133710 | GEO

The central nervous system-restricted transcription factor Olig2 opposes p53 responses to genotoxic damage in neural progenitors and malignant glioma.

Project description:High-grade gliomas are notoriously insensitive to radiation and genotoxic drugs. Paradoxically, the p53 gene is structurally intact in the majority of these tumors. Resistance to genotoxic modalities in p53-positive gliomas is generally attributed to attenuation of p53 functions by mutations of other components within the p53 signaling axis, such as p14(Arf), MDM2, and ATM, but this explanation is not entirely satisfactory. We show here that the central nervous system (CNS)-restricted transcription factor Olig2 affects a key posttranslational modification of p53 in both normal and malignant neural progenitors and thereby antagonizes the interaction of p53 with promoter elements of multiple target genes. In the absence of Olig2 function, even attenuated levels of p53 are adequate for biological responses to genotoxic damage.

| S-EPMC3070398 | biostudies-literature

GLI3 binding regions in mouse embryonic forelimb buds

Project description:GLI3 binding regions in mouse embryonic forelimb buds

| PRJNA552300 | ENA

Olig2+ neuroepithelial motoneuron progenitors are not multipotent stem cells in vivo.

Project description:Neurons and glia are thought to arise from multipotent and self-renewing stem cells, which comprise the majority of neuroepithelial cells in the ventricular zone (VZ) of the early embryonic CNS. However, this idea remains to be tested rigorously, because CNS stem cells have been identified only by using in vitro assays, from which their abundance in vivo cannot be directly inferred. In the hematopoietic system, stem cells are characterized by using prospective isolation and direct in vivo transplantation. Here we have used this approach to ask whether most VZ progenitors behave as stem cells in vivo. The best-studied region of the embryonic CNS for addressing this problem is, arguably, the ventral spinal cord, within which progenitors in the motoneuron progenitor (pMN) domain sequentially generate motoneurons (MNs) and oligodendrocyte precursors (OPs). Virtually all VZ cells in pMN express the transcription factor Olig2. If most of these cells are stem cells, then they should maintain neurogenic potential, even at later, gliogenic stages. To test this hypothesis, we have prospectively isolated Olig2(+) cells from murine embryonic day (E)9.5 and E13.5 spinal cord and directly transplanted them to E2 chick spinal cord. Transplanted E9.5 cells generate both neurons, including MNs and OPs, whereas E13.5 cells generate. The observation that most Olig2(+) progenitors do not maintain neurogenic potential into the period of gliogenesis argues that they do not self-renew. These results do not support the commonly held view that most neuroepithelial cells in the embryonic CNS VZ are stem cells in vivo.

| S-EPMC1345718 | biostudies-literature

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