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Pax6 occupancy and expression profiling of wild type and Pax6 null neural progenitors

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

ORGANISM(S): Mus musculus

PROVIDER: GSE75256 | GEO | 2016/05/02

SECONDARY ACCESSION(S): PRJNA302910

REPOSITORIES: GEO

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Pax6 occupancy and expression profiling of wild type and Pax6 null neural progenitors

Project description:Pax6 occupancy and expression profiling of wild type and Pax6 null neural progenitors

| PRJNA302910 | ENA

Expression data from wild type and Pax6 null neural progenitors

Project description:Pax6 is a highly conserved transcription factor among vertebrates and is important in various aspects of the central nervous system (CNS) development. However, the gene regulatory circuitry of Pax6 underlying these functions remains elusive. We find that, following expression in neural progenitor cells, Pax6 targets many promoters embedded in an active chromatin environment. Intriguingly, many of these sites are also bound by another progenitor factor, Sox2, which cooperates with Pax6 in gene regulation. A combinatorial analysis of Pax6 binding dataset with transcriptome changes in Pax6-deficient neural progenitors reveals a dual role for Pax6, in which it activates the neuronal (ectodermal) genes while concurrently represses the mesodermal and endodermal genes thereby ensuring the unidirectionality of lineage commitment towards glutamatergic neuronal differentiation. Furthermore, Pax6 is critical for inducing activity of transcription factors that elicit neurogenesis and repress others that promote non-neuronal lineages. In addition to many established downstream effectors, Pax6 directly binds and activates a number of genes that are specifically expressed in neural progenitors but have not been previously implicated in neurogenesis. The in utero knockdown of one such gene, Ift74, during brain development impairs polarity and migration of new-born neurons. These findings demonstrate new aspects of the gene regulatory circuitry of Pax6, revealing how it functions to control neuronal development at multiple levels to ensure unidirectionality and proper execution of the neurogenic program.

2016-05-02 | GSE75252 | GEO

E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-08-31 | GSE32355 | GEO

Sequencing Facilitates Quantitative Analysis of lncSync-null and wild-type mouse heart cardiomyocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

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CHD8 regulates neurodevelopmental pathways associated with autism spectrum disorder in neural progenitors

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

2014-10-07 | E-GEOD-61492 | biostudies-arrayexpress

Gene Expression Profiling in Wild-Type and PPARα-Null Mice Exposed to Perfluorooctane Sulfonate Reveals PPARα-Independent Effects.

Project description:Perfluorooctane sulfonate (PFOS) is a perfluoroalkyl acid (PFAA) and a persistent environmental contaminant found in the tissues of humans and wildlife. Although blood levels of PFOS have begun to decline, health concerns remain because of the long half-life of PFOS in humans. Like other PFAAs, such as, perfluorooctanoic acid (PFOA), PFOS is an activator of peroxisome proliferator-activated receptor-alpha (PPARα) and exhibits hepatocarcinogenic potential in rodents. PFOS is also a developmental toxicant in rodents where, unlike PFOA, its mode of action is independent of PPARα. Wild-type (WT) and PPARα-null (Null) mice were dosed with 0, 3, or 10 mg/kg/day PFOS for 7 days. Animals were euthanized, livers weighed, and liver samples collected for histology and preparation of total RNA. Gene profiling was conducted using Affymetrix 430_2 microarrays. In WT mice, PFOS induced changes that were characteristic of PPARα transactivation including regulation of genes associated with lipid metabolism, peroxisome biogenesis, proteasome activation, and inflammation. PPARα-independent changes were indicated in both WT and Null mice by altered expression of genes related to lipid metabolism, inflammation, and xenobiotic metabolism. Such results are similar to studies done with PFOA and are consistent with modest activation of the constitutive androstane receptor (CAR), and possibly PPARγ and/or PPARβ/δ. Unique treatment-related effects were also found in Null mice including altered expression of genes associated with ribosome biogenesis, oxidative phosphorylation, and cholesterol biosynthesis. Of interest was up-regulation of Cyp7a1, a gene which is under the control of various transcription regulators. Hence, in addition to its ability to modestly activate PPARα, PFOS induces a variety of PPARα-independent effects as well.

| S-EPMC2948942 | biostudies-literature

Transcriptomic and Chromatin Landscape Analysis of Wild Type and FOXA2-/- ES-derived Pancreatic Progenitors

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-05-14 | GSE114102 | GEO

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

In vitro modeling of glioblastoma initiation using PDGF-AA and p53-null neural progenitors.

Project description:BackgroundImagining ways to prevent or treat glioblastoma (GBM) has been hindered by a lack of understanding of its pathogenesis. Although overexpression of platelet derived growth factor with two A-chains (PDGF-AA) may be an early event, critical details of the core biology of GBM are lacking. For example, existing PDGF-driven models replicate its microscopic appearance, but not its genomic architecture. Here we report a model that overcomes this barrier to authenticity.MethodsUsing a method developed to establish neural stem cell cultures, we investigated the effects of PDGF-AA on subventricular zone (SVZ) cells, one of the putative cells of origin of GBM. We microdissected SVZ tissue from p53-null and wild-type adult mice, cultured cells in media supplemented with PDGF-AA, and assessed cell viability, proliferation, genome stability, and tumorigenicity.ResultsCounterintuitive to its canonical role as a growth factor, we observed abrupt and massive cell death in PDGF-AA: wild-type cells did not survive, whereas a small fraction of null cells evaded apoptosis. Surviving null cells displayed attenuated proliferation accompanied by whole chromosome gains and losses. After approximately 100 days in PDGF-AA, cells suddenly proliferated rapidly, acquired growth factor independence, and became tumorigenic in immune-competent mice. Transformed cells had an oligodendrocyte precursor-like lineage marker profile, were resistant to platelet derived growth factor receptor alpha inhibition, and harbored highly abnormal karyotypes similar to human GBM.ConclusionThis model associates genome instability in neural progenitor cells with chronic exposure to PDGF-AA and is the first to approximate the genomic landscape of human GBM and the first in which the earliest phases of the disease can be studied directly.

| S-EPMC7594559 | biostudies-literature

Pax6 mutant neocortex vs. wild type

Project description:Pax6 is a transcription factor with key functional roles in embryonic development. In order to identify downstream effectors of Pax6 in the developing cerebral cortex we performed microarray analysis. We compared gene expression profiles of cortical tissues isolated from wild type and Pax6-/- mouse embryos.

2011-10-31 | GSE32271 | GEO

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