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Transcriptome changes in Olig2-3 over-expression retina ganglion cells (RGCs) by AAV-Olig1/2.

ABSTRACT: To gain mechanistic insights into the effects of Olig family, we performed gene expression profiling analysis in RGCs. Transcriptome changes in Olig1-3 over-expression RGCs showed up-regulating genes related to axon projection development and regeneration-associated genes (RAGs), such as Stmn2, Gal, Gap43, and Sprr1a.

ORGANISM(S): Mus musculus

PROVIDER: GSE261812 | GEO | 2024/04/30

REPOSITORIES: GEO

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Transcriptome changes in Olig1 over-expression retina ganglion cells (RGCs) by AAV-Olig1

Project description:To gain mechanistic insights into the effects of Olig1, we performed gene expression profiling analysis in RGCs. Transcriptome changes in Olig1 over-expression RGCs showed up-regulating genes related to axon projection development and regeneration-associated genes (RAGs), such as Stmn2, Gal, Gap43, and Sprr1a.

2022-12-30 | GSE221116 | GEO

Transcriptome changes in Olig1 over-expression retina ganglion cells (RGCs) by AAV-Olig1

Project description:Transcriptome changes in Olig1 over-expression retina ganglion cells (RGCs) by AAV-Olig1

| PRJNA912849 | ENA

Transcriptome changes in Olig2-3 over-expression retina ganglion cells (RGCs) by AAV-Olig1/2.

Project description:Transcriptome changes in Olig2-3 over-expression retina ganglion cells (RGCs) by AAV-Olig1/2.

| PRJNA1089135 | ENA

ID4 function antagonizes OLIG1 and OLIG2 to suppressive aggressive glioma

Project description:The basic helix-loop-helix proteins Olig1 and Olig2 are expressed in high grade, aggressive human glioblastoma multiformes (GBMs). Here we investigated genetic mechanisms regulating Olig1/2 function during gliomagenesis. Although Olig2 function is necessary for early-aggressive tumor formation in a genetically relevant model of classic GBMs with intact p53 function, late-onset gliomas do eventually form. Using an unbiased approach, we identified Id4, encoding a negative HLH protein, as a gene target potently repressed by Olig2 in glioma progenitors. Although Id4 is thought to antagonize proneural genes involved in differentiation, we report a paradoxical role for Id4 in glioma. Genetic deletion of Id4 converts Olig2-/- gliomas to the early-aggressive form, and conversely, overexpression of Id4 inhibits intact Olig2 and prevents even late-onset tumors. Olig1 overexpression is sufficient for gliomagenesis in an Id4-dependent manner. Together, these findings indicate that gliomagenic factors Olig1 and Olig2 are opposed by Id4 function, which acts as tumor suppressor in p53-intact gliomas.

2018-01-02 | GSE44151 | GEO

Expression analysis of neural stem cells isolated from Olig1-wt and Olig1-ko embryos

Project description:Olig1 is a bHLH transcription factor which is important for Oligodendrocyte development We used microarray profiling to assess which genes are differentially expressed in absence of Olig1 in neural stem cells. Neural stem cells were isolated from ganglionic eminences of E14.5 wild-type and Olig1-KO brains. The cells were cultured in serum-free neural stem cell media and RNA extracted.

2012-07-27 | E-GEOD-39706 | biostudies-arrayexpress

Expression analysis of neural stem cells isolated from Olig1-wt and Olig1-ko embryos

2012-07-28 | GSE39706 | GEO

Separated at birth? The functional and molecular divergence of OLIG1 and OLIG2.

Project description:The basic helix-loop-helix transcription factors oligodendrocyte transcription factor 1 (OLIG1) and OLIG2 are structurally similar and, to a first approximation, coordinately expressed in the developing CNS and postnatal brain. Despite these similarities, it was apparent from early on after their discovery that OLIG1 and OLIG2 have non-overlapping developmental functions in patterning, neuron subtype specification and the formation of oligodendrocytes. Here, we summarize more recent insights into the separate roles of these transcription factors in the postnatal brain during repair processes and in neurological disease states, including multiple sclerosis and malignant glioma. We discuss how the unique functions of OLIG1 and OLIG2 may reflect their distinct genetic targets, co-regulator proteins and/or post-translational modifications.

| S-EPMC3733228 | biostudies-literature

Olig1 is a Smad cofactor involved in cell motility induced by transforming growth factor-b

Project description:Transforming growth factor (TGF)-Î² plays crucial roles in embryonic development and adult tissue homeostasis by eliciting various cellular responses in target cells. TGF-Î² signaling is principally mediated through receptor-activated Smad proteins, which regulate expression of target genes in cooperation with other DNA-binding transcriptionfactors (Smad cofactors). In this study, we found that the basic helix-loop-helix transcription factor Olig1 is a Smad cofactor involved in TGF-b-induced cell motility. Knockdown of Olig1 attenuated TGF-Î²-induced cell motility in chamber migration and wound healing assays. In contrast, Olig1 knockdown had no effect on bone morphogenetic protein-induced cell motility, TGF-Î²-induced cytostasis or epithelial-mesenchymal transition. Furthermore, we observed that cooperation of Smad2/3 with Olig1 is regulated by a peptidyl-prolyl cis/trans isomerase, Pin1. TGF-b-induced cell motility, induction of Olig1-regulated genes, and physical interaction between Smad2/3 and Olig1 were all inhibited after knockdown of Pin1, indicating a novel mode of regulation of Smad signaling. We also found that Olig1 interacts with the L3 loop of Smad3. Using a synthetic peptide corresponding to the L3 loop of Smad3, we succeeded in selectively inhibiting TGF-b-induced cell motility. These findings may lead to a new strategy for selective regulation of TGF-b-induced cellular responses. NMuMG cells were transfected with siRNAs (siControl, siOlig1 or siPin1) and treated with or without TGF-b for 1h. We compared genes affected by knockdown of Olig1 and that of Pin1.

2013-07-01 | E-GEOD-46405 | biostudies-arrayexpress

Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome.

Project description:Over-inhibition is thought to be one of the underlying causes of the cognitive deficits in Ts65Dn mice, the most widely used model of Down syndrome. We found a direct link between gene triplication and defects in neuron production during embryonic development. These neurogenesis defects led to an imbalance between excitatory and inhibitory neurons and to increased inhibitory drive in the Ts65Dn forebrain. We discovered that Olig1 and Olig2, two genes that are triplicated in Down syndrome and in Ts65Dn mice, were overexpressed in the Ts65Dn forebrain. To test the hypothesis that Olig triplication causes the neurological phenotype, we used a genetic approach to normalize the dosage of these two genes and thereby rescued the inhibitory neuron phenotype in the Ts65Dn brain. These data identify seminal alterations during brain development and suggest a mechanistic relationship between triplicated genes and these brain abnormalities in the Ts65Dn mouse.

| S-EPMC3249618 | biostudies-other

Olig1 is a Smad cofactor involved in cell motility induced by transforming growth factor-b

Project description:Transforming growth factor (TGF)-β plays crucial roles in embryonic development and adult tissue homeostasis by eliciting various cellular responses in target cells. TGF-β signaling is principally mediated through receptor-activated Smad proteins, which regulate expression of target genes in cooperation with other DNA-binding transcriptionfactors (Smad cofactors). In this study, we found that the basic helix-loop-helix transcription factor Olig1 is a Smad cofactor involved in TGF-b-induced cell motility. Knockdown of Olig1 attenuated TGF-β-induced cell motility in chamber migration and wound healing assays. In contrast, Olig1 knockdown had no effect on bone morphogenetic protein-induced cell motility, TGF-β-induced cytostasis or epithelial-mesenchymal transition. Furthermore, we observed that cooperation of Smad2/3 with Olig1 is regulated by a peptidyl-prolyl cis/trans isomerase, Pin1. TGF-b-induced cell motility, induction of Olig1-regulated genes, and physical interaction between Smad2/3 and Olig1 were all inhibited after knockdown of Pin1, indicating a novel mode of regulation of Smad signaling. We also found that Olig1 interacts with the L3 loop of Smad3. Using a synthetic peptide corresponding to the L3 loop of Smad3, we succeeded in selectively inhibiting TGF-b-induced cell motility. These findings may lead to a new strategy for selective regulation of TGF-b-induced cellular responses.

2013-07-01 | GSE46405 | GEO

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