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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE76411 | GEO | 2016/02/21

SECONDARY ACCESSION(S): PRJNA307591

REPOSITORIES: GEO

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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

Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (RNA-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. Gene expression profiling of optic nerve from P12 control and Hdac3 cKO mice

2016-02-21 | E-GEOD-76410 | biostudies-arrayexpress

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

2016-02-21 | GSE76410 | GEO

CD133/CD140a-Based Isolation of Distinct Human Multipotent Neural Progenitor Cells and Oligodendrocyte Progenitor Cells

Project description:The mechanisms underlying the specification of oligodendrocyte fate from multipotent neural progenitor cells (NPCs) in developing human brain are unknown. In this study, we sought to identify antigens sufficient to distinguish NPCs free from oligodendrocyte progenitor cells (OPCs). We investigated the potential overlap of NPC and OPC antigens using multicolor fluorescence-activated cell sorting (FACS) for CD133/PROM1, A2B5, and CD140a/PDGFaR antigens. Surprisingly, we found that CD133, but not A2B5, was capable of enriching for OLIG2 expression, Sox10 enhancer activity, and oligodendrocyte potential. As a subpopulation of CD133- positive cells expressed CD140a, we asked whether CD133 enriched bone fide NPCs regardless of CD140a expression. We found that CD133+CD140a- cells were highly enriched for neurosphere initiating cells and were multipotent. Importantly, when analyzed immediately following isolation, CD133+CD140a- NPCs lacked the capacity to generate oligodendrocytes. In contrast, CD133+CD140a+ cells were OLIG2-expressing OPCs capable of oligodendrocyte differentiation, but formed neurospheres with lower efficiency and were largely restricted to glial fate. Gene expression analysis further confirmed the stem cell nature of CD133+CD140a- cells. As human CD133+ cells comprised both NPCs and OPCs, CD133 expression alone cannot be considered a specific marker of the stem cell phenotype, but rather comprises a heterogeneous mix of glial restricted as well as multipotent neural precursors. In contrast, CD133/CD140a-based FACS permits the separation of defined progenitor populations and the study of neural stem and oligodendrocyte fate specification in the human brain. 12 samples, 4 groups (FACS-sorted cell populations),3 replicates in each group, each replicate is from a separate patient sample

2013-04-23 | E-GEOD-40676 | biostudies-arrayexpress

Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch

Project description:Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch

| PRJNA307590 | ENA

CD133/CD140a-Based Isolation of Distinct Human Multipotent Neural Progenitor Cells and Oligodendrocyte Progenitor Cells

2013-04-23 | GSE40676 | GEO

Astrocyte-Oligodendrocyte interaction regulates central nervous system regeneration

Project description:Failed regeneration of myelin around neuronal axons following central nervous system damage contributes to nerve dysfunction and clinical decline in various neurological conditions, for which there is an unmet therapeutic demand. Here, we show that interaction between glial cells – astrocytes and mature myelin-forming oligodendrocytes – is a critical determinant of remyelination. Using in vivo/ ex vivo/ in vitro rodent models and human brain lesion analyses, we discover that astrocytes support the survival of regenerating oligodendrocytes, via downregulation of the Nrf2 pathway associated with increased astrocytic cholesterol biosynthesis pathway activation. Remyelination fails following sustained astrocytic Nrf2 activation in focally-lesioned mice yet is restored by either cholesterol biosynthesis/efflux stimulation, or Nrf2 inhibition using the existing therapeutic Luteolin. We identify that astrocyte-oligodendrocyte interaction regulates remyelination, and reveal a drug strategy for central nervous system regeneration centred on targeting this interaction.

2023-05-17 | PXD041850 | Pride

Transcription profiling of mouse ventral forebrain cells in neuronal-glial fate specification and oligodendrocyte lineage maturation

Project description:This experiment compared the expression of mRNAs and noncoding RNAs during neuronal-glial fate specification and oligodendrocyte lineage maturation. The primary aim of the experiment was to identify ncRNAs that were differentially expressed during this process.

2010-01-07 | E-TABM-874 | biostudies-arrayexpress

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

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

2013-01-20 | GSE42447 | GEO

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