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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE42447 | GEO | 2013/01/20

SECONDARY ACCESSION(S): PRJNA182002

REPOSITORIES: GEO

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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/?-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

Seh1 Interacts with Olig2 and Brd7 to Promote Oligodendrocyte Differentiation and Myelination (ATAC_Seq)

Project description:Nuclear pore complex components (Nups) are involved in neural development and alterations in Nup genes are linked to human neurological diseases. However, the physiological functions of specific Nups and the underlying mechanisms involved in these processes remain elusive. Here we show that tissue-specific depletion of nucleoporin Seh1 causes dramatic myelination defects in the Central Nervous System (CNS). Seh1-deficient Oligodendrocyte Progenitor Cells (OPCs) proliferate properly, but fail to differentiate into mature oligodendrocytes, which impairs myelin production and remyelination after demyelinating injury. Genome-wide analyses show that Seh1 regulates a core myelinogenic regulatory network and depletion of Seh1 alters open chromatin configurations at its target genes. Mechanistically, Seh1 regulates OPCs differentiation by assembling Olig2 and Brd7 into a transcription complex at nuclear pores. Together, our results reveal that Seh1 is required for oligodendrocyte differentiation and myelination by promoting assembly of an Olig2-dependent transcription complex and expose nucleoporins as key players in the CNS.

2018-09-12 | GSE119815 | GEO

Seh1 Interacts with Olig2 and Brd7 to Promote Oligodendrocyte Differentiation and Myelination (ChIP-Seq)

2018-09-12 | GSE119814 | GEO

Seh1 Interacts with Olig2 and Brd7 to Promote Oligodendrocyte Differentiation and Myelination (RNA-Seq)

2018-09-12 | GSE119812 | GEO

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [ChIP-seq]

Project description:Mutations in CHD7, encoding ATP-dependent chromodomain-helicase-DNA-binding protein 7, in CHARGE syndrome leads to multiple congenital anomalies including growth retardation, craniofacial malformations and neurological dysfunction. Currently, mechanisms underlying the CNS phenotypes remain poorly understood. Here, we show that Chd7 is a direct transcriptional target of oligodendrogenesis-promoting factors Olig2 and Brg1 and required for proper timing of CNS myelination and remyelination. Genome-occupancy analyses coupled with transcriptome profiling reveal that Chd7 cooperates with Sox10 to target the enhancers of key myelinogenic genes, and identify novel Chd7 target. Examination of Chd7 and Sox10 genomewide occupancy in differentiating oligodendrocytes

2016-02-29 | E-GEOD-72725 | biostudies-arrayexpress

Newfound roles of OLIG2 in the regulation of lncRNAs, epigenetic status and its own expression at transcriptional and post-transcriptional levels during oligodendrocyte lineage formation

Project description:We performed an integrated study of genome-wide OLIG2 binding and the epigenetic modification status of both coding and non-coding genes during three stages of oligodendrocyte differentiation in vivo: Neural Stem Cells (NSC), Oligodendrocyte Progenitor Cells (OPC), and Newly Formed Oligodendrocytes (NFO). We found that 613 lncRNAs have OLIG2-binding sites and are expressed in at least one cell type, which can potentially be activated or repressed by OLIG2. 48 of them have increased expression in oligodendrocyte lineage cells. Predicting lncRNA functions by using a “guilt-by-association” approach revealed that the functions of these 48 lncRNAs were enriched in ‘oligodendrocyte development and differentiation’. Additionally, bivalent genes are known to play essential roles during embryonic stem cell differentiation. We identified bivalent genes in NSC, OPC, and NFO, and found that some bivalent genes bound by OLIG2 are dynamically regulated during oligodendrocyte development. Importantly, we have identified AU-rich elements (AREs) in the 3’-UTRs of Olig2 mRNAs. We unveiled a previously unknown mechanism that, in addition to transcriptional regulation via DNA binding, OLIG2 could post-transcriptionally self-regulate expression through interaction with the 3’-UTR of its own mRNA.

2021-07-08 | GSE155890 | GEO

Olig2 ablation in immature oligodendrocytes does not enhance CNS myelination and remyelination

Project description:The oligodendrocyte (OL) lineage gene Olig2 persistently expresses throughout oligodendroglial development and required for oligodendroglial specification and differentiation. Here, Together, by leveraging multiple immature OL-expressing Cre lines at different stages, we demonstrate that Olig2 is required for differentiation and myelination of immature OL and myelin repair and raise fundamental questions about the previously proposed role for Olig2 in opposing OL myelination, while highlighting the importance of using Cre-dependent reporter for lineage tracing in studying cell fate transition.

2022-11-23 | GSE194258 | GEO

Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (ChIP-Seq)

Project description:Establishment and maintenance of CNS glial cell identity ensures proper brain development and function, yet the epigenetic mechanisms underlying glial fate control remain poorly understood. Here we show that the histone deacetylase Hdac3 controls oligodendrocyte-specification gene Olig2 expression, and functions as a molecular switch for oligodendrocyte and astrocyte lineage determination. Our data suggest that Hdac3 cooperates with p300 to prime and maintain oligodendrogenic programs while inhibiting Stat3-mediated astrogliogenesis, and thereby regulate phenotypic commitment at the point of oligodendrocyte-astrocytic fate decision. Examination of Hdac3 and p300 genomewide occupancy in differentiating oligodendrocytes

2016-02-21 | E-GEOD-76411 | biostudies-arrayexpress

Comparing the transcriptoms of Mettl14fl/fl and Mettl14 fl/fl; Olig2-Cre oligodendrocyre precursor cell (OPCs) and mature oligodendrocytes using Next Generation Sequencing

Project description:The goal of the experiment is to determine the transcriptome alternation of Mettl14 gene inactivation in different oligodendrocyte lineage cells(OPCs and mature oligodendrocytes), by comparing the Mettl14 fl/fl; Olig2-Cre(mutant) and Mettl14fl/fl(control) OPC and mature oligodendrocyte transcriptoms. Method: RNA collected from Mettl14fl/fl control and Mettl14fl/fl;Olig2-Cre OPC and oligodendrocytes was collected by standard protocols, sequenced using next generation high throughput sequencing technology, and processed in triplicate to produce a transcriptome profile deliminating the variable gene expression in the mutant cells. Results: We identified 11809 transcripts present in the OPC transcriptome, 586 were significantly upregulated and 177 were significantly downregulated in the mutant cells; Among 12,542 transcripts present in mature oligodendrocytes, 1388 transcripts were upregulated and 1247 were downregulated in the mutant cells(significance: q-value<0.001; fold changes (FC) that exceed 2.0 fold (log2 |FC|>1) in expression and an expression level that exceeds two counted transcripts per million (log2 |CPM| >1)) Conclusions: Mettl14 ablation differentially alters the OPC and oligodendrocyte transcriptomes

2019-12-31 | GSE124243 | GEO

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