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Coordinated Regulation of Cortical Astrocyte Maturation by OLIG1 and OLIG2 through BMP7 Signaling Modulation

ABSTRACT: Coordinated Regulation of Cortical Astrocyte Maturation by OLIG1 and OLIG2 through BMP7 Signaling Modulation

PROVIDER: PRJNA1190380 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31488775_1.fastq.gz	Fastqsanger.gz
	SRR31488775_2.fastq.gz	Fastqsanger.gz

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Coordinated Regulation of Cortical Astrocyte Maturation by OLIG1 and OLIG2 through BMP7 Signaling Modulation

Project description:Astrocyte maturation is crucial for brain function, yet the mechanisms regulating this process remain poorly understood. In this study, we identify the bHLH transcription factors Olig1 and Olig2 as essential coordinators of cortical astrocyte maturation. We demonstrate that Olig1 and Olig2 work synergistically to regulate cortical astrocyte maturation by modulating BMP7 expression. Genetic ablation of both Olig1 and Olig2 results in defective astrocyte morphology, including reduced process complexity, and an immature gene expression profile. Single-cell RNA sequencing reveals a shift towards a less mature astrocyte state, marked by elevated levels of HOPX and GFAP, resembling human astrocytes. Mechanistically, Olig1 and Olig2 bind directly to the Bmp7 enhancer, repressing its expression to promote astrocyte maturation. Overexpression of Bmp7 in vivo replicates the astrocyte defects seen in Olig1/2 double mutants, confirming the critical role of BMP7 signaling in this process. These findings provide new insights into the transcriptional and signaling pathways regulating astrocyte development and highlight Olig1 and Olig2 as key regulators of cortical astrocyte maturation, with potential implications for understanding glial dysfunction in neurological diseases.

2024-11-30 | GSE282764 | GEO

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

Genome-wide mapping of Olig2 targets in primary oligodendrocytes

Project description:Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/?-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and ?-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair. ChIP-seq was performed to identify Olig2 direct target genes in oligodendrocytes during oligodendrocyte differentiation.

2012-08-31 | E-GEOD-40506 | biostudies-arrayexpress

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

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

Project description: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.

2024-04-30 | GSE261812 | 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

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

Activation of the chromatin-remodeling factor Smarca4/Brg1 cooperates with Olig2 to establish oligodendrocyte identity and control CNS myelination [ChIP-seq]

Project description:We investigate the role of Brg1 and Olig2 during oligodendrocyte differentiation by combining gene conditional knockout and next generation sequencing technology. We generate genome-wide maps of RNA polymerase II (RPolII), Brg1 (Smarca4), Olig2 and histone modifications in primary rat oligodendrocyte precursor cells (iOLs), differentiating oligodendrocytes and mature oligodendrocytes.We found that Brg1 is intensely regulated by RPolII at the initiation of oligodedrocyte differentiation. The genomic distribution of Brg1 in differentiating oligodendrocytes is pre-directed by Olig2 in iOLs. The dynamic interaction of Brg1 and chromatin is correlate with the distinct stages of gene expression during maturation. Finally, we show that Brg1 and Olig2 localization predict critical genes controling CNS myeliantion. Our study represents the first detailed analysis of genomic landscape during the oligodendrocyte development and provides a framework for further understanding of molecular mechanisms underlying oligodendrocyte lineage progression. Genomic distribution of Brg1, Olig2, RPolII and three different histone modifications in three oligodendrocyte developemtal stages were examined using primary cells by ChIP-sequencing. Spinal cord mRNA profiles of 14-day old control and Brg1c/c;Olig1-Cre mice were generated by RNA-sequencing.

2013-01-20 | E-GEOD-42447 | biostudies-arrayexpress

Genome-wide mapping of Olig2 targets in primary oligodendrocytes

Project description:Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/β-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and β-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair.

2012-08-31 | GSE40506 | GEO

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