Genome-wide identification of target genes for the transcription factor Klf13 in differentiated primary mouse oligodendrocytes.
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ABSTRACT:
PROVIDER: PRJNA877105 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21437478_1.fastq.gz | Fastqsanger.gz | |||
| SRR21437478_2.fastq.gz | Fastqsanger.gz | |||
| SRR21437479_1.fastq.gz | Fastqsanger.gz | |||
| SRR21437479_2.fastq.gz | Fastqsanger.gz | |||
| SRR21437480_1.fastq.gz | Fastqsanger.gz |
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Project description:To identify target genes of the Klf13 transcription factor in oligodendroglia in a genome-wide and unbiased approach, we cultured primary mouse oligodendroglia of wild type and Klf13-knockout mice, kept them under differentiating conditions, and isolated total RNA which was followed by RNA-Seq studies. Among others we detected substantial changes in the expression of genes associated with differentiation and myelination of oligodendrocytes.
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Project description:Genome-wide identification of target genes for the transcription factors Sox2 and Sox3 in differentiated primary mouse oligodendrocytes
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Project description:To identify target genes of the transcription factors Sox2 and Sox3 in oligodendroglia in a genome-wide and unbiased approach, we cultured primary mouse oligodendroglia of wild type mice and mice with floxed alleles for Sox2 and Sox3, treated the cells with Tat-Cre to induce recombination, then kept cells under differentiating conditions, and isolated total RNA for RNA-Seq studies. Among others we detected substantial changes in the expression of genes associated with the onset of terminal differentiation of oligodendrocytes.
2024-06-03 | GSE263925 | GEO
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
Project description:Macrophages are differentiated from human circulating monocytes using M-CSF and GM-CSF. Oligodendrocytes are differentiated from human oligodendrocyte precursopr cells (#1610, ScienCell) using oligodendrocyte precursor cell differentiation medium.
2018-03-08 | GSE104742 | GEO
Project description:Oligodendrocytes undergo extensive changes as they differentiate from progenitors into myelinating cells. To better understand the molecular mechanisms underlying this transformation, we performed a comparative analysis using gene expression profiling of A2B5+ oligodendrocyte progenitors and O4+ oligodendrocytes. Cells were sort-purified ex vivo from postnatal rat brain using flow cytometry. Using Affymetrix microarrays, 1707 transcripts were identified with a more than twofold increase in expression inO4+oligodendrocytes. Many genes required for oligodendrocyte differentiation were upregulated in O4+ oligodendrocytes, including numerous genes encoding myelin proteins. Transcriptional changes included genes required for cell adhesion, actin cytoskeleton regulation, and fatty acid and cholesterol biosynthesis. At the O4+ stage, there was an increase in expression of a novel proline-rich transmembrane protein (Prmp). Localized to the plasma membrane, Prmp displays adhesive properties that may be important for linking the extracellular matrix to the actin cytoskeleton. Together, our results highlight the usefulness of this discovery-driven experimental strategy to identify genes relevant to oligodendrocyte differentiation and myelination. Keywords: develepmental stage, oligodendrocyte differentiation
2006-09-30 | GSE5940 | GEO
Project description:To identify target genes of the transcription factors Sox8 and Sox10 in oligodendrocytes in a genome-wide and unbiased approach, we induced oligodendocyte-specific deletion of Sox8, Sox10 or a combination thereof (Sox8 knockout, Sox10 knockout, double knockout) in 2 months-old mice, dissected the corpus callosum of control and mutant mice after 21 days and isolated total RNA for ensuing RNA-Seq studies. Among others we detected substantial changes in the expression of genes associated with differentiation of oligodendrocytes and myelination in Sox10 knockout mice as well as double knockout mice but not in Sox8 knockout mice.
2024-08-28 | GSE269122 | GEO
Project description:Krüppel-like factors (KLFs) play key roles in nervous system development and function. Several KLFs are known to promote, and then maintain neural cell differentiation. Our previous work focused on the actions of KLF9 in mouse hippocampal neurons. Here we investigated genomic targets and functions of KLF9’s paralog KLF13, with the goal of understanding how these two closely related transcription factors influence hippocampal cell function, proliferation, survival and regeneration. We engineered the adult mouse hippocampus-derived cell line HT22 to control Klf13 expression with doxycycline. We also generated HT22 Klf13 knock out cells, and we analyzed primary hippocampal cells from wild type and Klf13-/- mice. RNA sequencing showed that KLF13, like KLF9, acts predominantly as a transcriptional repressor in hippocampal neurons and can regulate other Klf genes. Pathway analysis revealed that genes regulated by KLF13 are involved in cell cycle, cell survival, cytoarchitecture regulation, among others. Chromatin-streptavidin sequencing conducted on chromatin isolated from HT22 cells expressing biotinylated KLF13 identified 9506 genomic targets; 79% were located 1 kilobase upstream of transcription start sites. Transfection-reporter assays confirmed that KLF13 can directly regulate transcriptional activity of its target genes. Comparison of the target genes of KLF9 and KLF13 found that they share some functions that were likely present in their common ancestor, but have also acquired distinct functions during evolution. Flow cytometry showed that KLF13 promotes cell cycle progression, and it protects cells from glutamate-induced excitotoxic damage. Taken together, our findings establish novel roles and molecular mechanisms for KLF13 actions in mammalian hippocampal neurons.
2020-04-09 | GSE148383 | GEO
Project description:Oligodendrocytes have recently been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS). Here we differentiated fibroblasts into induced neural progenitors and subsequently into oligodendrocytes and astrocytes. To confirm that the cells obtained with this protocol express the gene signature of oligodendrocytes, we performed a small gene expression study limited to four iOligodendrocyte lines from two controls (nos. 155 and 170) and two patients (nos. 12 and 17), four iAstrocyte lines from the same samples, and four fibroblast lines from one of our previously published studies
2016-10-10 | GSE87385 | GEO
Project description:BACKGROUND: The polycomb group protein Ezh2 is an epigenetic repressor of transcription originally found to prevent untimely differentiation of pluripotent embryonic stem cells. We previously demonstrated that Ezh2 is also expressed in multipotent neural stem cells (NSCs). We showed that Ezh2 expression is downregulated during NSC differentiation into astrocytes or neurons. However, high levels of Ezh2 remained present in differentiating oligodendrocytes until myelinating. This study aimed to elucidate the target genes of Ezh2 in NSCs and in premyelinating oligodendrocytes (pOLs). METHODOLOGY/PRINCIPAL FINDINGS: We performed chromatin immunoprecipitation followed by high-throughput sequencing to detect the target genes of Ezh2 in NSCs and pOLs. We found 1532 target genes of Ezh2 in NSCs. During NSC differentiation, the occupancy of these genes by Ezh2 was alleviated. However, when the NSCs differentiated into oligodendrocytes, 393 of these genes remained targets of Ezh2. Analysis of the target genes indicated that the repressive activity of Ezh2 in NSCs concerns genes involved in stem cell maintenance, in cell cycle control and in preventing neural differentiation. Among the genes in pOLs that were still repressed by Ezh2 were most prominently those associated with neuronal and astrocytic committed cell lineages. Suppression of Ezh2 activity in NSCs caused loss of stem cell characteristics, blocked their proliferation and ultimately induced apoptosis. Suppression of Ezh2 activity in pOLs resulted in derangement of the oligodendrocytic phenotype, due to re-expression of neuronal and astrocytic genes, and ultimately in apoptosis. CONCLUSIONS/SIGNIFICANCE: Our data indicate that the epigenetic repressor Ezh2 in NSCs is crucial for proliferative activity and maintenance of neural stemness. During differentiation towards oligodendrocytes, Ezh2 repression continues particularly to suppress other neural fate choices. Ezh2 is completely downregulated during differentiation towards neurons and astrocytes allowing transcription of these differentiation programs. The specific fate choice towards astrocytes or neurons is apparently controlled by epigenetic regulators other than Ezh2. Examination of Ezh2 target sites in 2 different primary cells types
2012-07-30 | E-GEOD-31655 | biostudies-arrayexpress