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Molecular cause of the differential activity of Sox8 and Sox10 in oligodendroglial cells

ABSTRACT: Molecular cause of the differential activity of Sox8 and Sox10 in oligodendroglial cells

PROVIDER: PRJNA1178290 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31130818.fastq.gz	Fastqsanger.gz
	SRR31130819.fastq.gz	Fastqsanger.gz
	SRR31130820.fastq.gz	Fastqsanger.gz
	SRR31130821.fastq.gz	Fastqsanger.gz
	SRR31130822.fastq.gz	Fastqsanger.gz

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Similar Datasets

Molecular cause of the differential activity of Sox8 and Sox10 in oligodendroglial cells

Project description:Oligodendroglial cells are responsible for the generation of myelin sheaths in the central nervous system and thereby render rapid saltatory conduction possible. During development, oligodendroglial cells express the three paralogous transcription factors Sox8, Sox9 and Sox10. In mature oligodendrocytes Sox8 and Sox10 expression persists. Whereas Sox9 and Sox10 fulfill important regulatory roles in these cells, Sox8 has only a limited impact on oligodendroglial development and myelination. By replacing Sox10 with Sox8 or Sox9 in the oligodendroglial Oln93 cell line and by comparing expression profiles, we show that Sox8 regulates the same processes as Sox10 and Sox9, but has a substantially lower transcriptional activity under standard culture conditions.

2025-01-02 | GSE280389 | GEO

Transcription factors Sox8 and Sox10 contribute differentially to maintenance of the differentiated state in oligodendrocytes

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

Determination of Sox10-regulated genes in the oligodendroglial precursor cell line OLN93

Project description:To determine Sox10-regulated genes in the oligodendroglial precursor cell line OLN93, CRISPR/Cas9-mediated genome editing was performed to inactivate Sox10. For CRISPR/Cas9-mediated Sox10 inactivation, two guide sequences (5’-GCTGCGAGCCAGCCCAGGGCC-3’ for clone A and 5’-GTTGCCCAATTCGCCG GGCCC-3’ for clone B) were separately cloned into pX330. Oln93 cells were co-transfected with pEGFP-N1 and the pX330 plasmids that express the respective guide RNA and SpCas9. Transfected GFP-positive cells were enriched by fluorescence activated cell-sorting and seeded at single cell density in 96-well plates. Homogeneously GFP-expressing clones were analysed for loss of Sox10 protein by immunocytochemistry. Clones without Sox10 protein were obtained with both guide RNAs. Sox10 inactivation was confirmed by Sanger sequencing of the Sox10 gene. RNA was isolated from one clone A and one clone B as well as two independent RNA samples of wildtype OLN93 cells and submitted to RNA-seq.

2019-12-15 | GSE136659 | GEO

Determination of Sox10-regulated genes in the oligodendroglial precursor cell line OLN93

Project description:Determination of Sox10-regulated genes in the oligodendroglial precursor cell line OLN93

| PRJNA562933 | ENA

Gene expression profiling in the white matter with oligodendroglial stage-specfic activation or inhibition of ErbB receptors

Project description:To gain insight of how ErbB signaling in oligodendroglial progenitor cell to newly-formed oligodendrocyte stages (OPC-NFOs) regulated adolescent oligodendroglial development, we did RNA-seq analyses of subcortical white matter tissues isolated from Sox10-ErbB2V664E mice or Sox10-dnEGFR mice and their littermate controls after doxycycline treatment, respectively. Both mice were revealed hypomyelination although OPC proliferation or survival were differently altered in them. For each group we sequenced three pairs of samples, and revealed 2298 genes that had altered expression in the white matter of Sox10-ErbB2V664E mice, as well as 1184 genes that had altered expression in that of Sox10-dnEGFR mice. By comparing the two groups of genes, we identified 50 genes which had opposite expression tendency in the two mouse lines which was potentially involved in ErbB signaling and contributed to regulation of OPC proliferation and survival. Meanwhile, we identified 68 genes which exhibited similar expression tendency in Sox10-ErbB2V664E and Sox10-dnEGFR mice which had potential in the regulation of central myelination.

2018-12-08 | GSE123491 | GEO

Transcription factors Sox8 and Sox10 contribute differentially to maintenance of the differentiated state in oligodendrocytes

Project description:Transcription factors Sox8 and Sox10 contribute differentially to maintenance of the differentiated state in oligodendrocytes

| PRJNA1120355 | ENA

Transcription profiling of mice mutant for Sox8 and Sox9 has early testicular sterility

Project description:To study a possible redundant role of mouse Sox8 and Sox9 after testis induction we generated double mutants by AMH-Cre conditional inactivation of Sox9 in a Sox8-/- background. Double mutants arrest spermatogenesis in early pubescence. We performed expression profiling to explore causes. AMH-Cre/+;Sox9flox/flox;Sox8-/- is a conditional homozygous knockout of SOX9 in a sox8-/- background, using an AMH-CRE line where the CRE recombinase is expressed under the promoter region of the human AMH gene in Sertoli cells starting at E13.5. The specific cross was between males of the genotype +/+;Sox9flox/flox;Sox8-/- and females of the genotype AMH-Cre/+;Sox9flox/flox;Sox8+/-.

2013-01-03 | E-TABM-531 | biostudies-arrayexpress

EHMT1 mediates cellular motility in embryonal rhabdomyosarcoma by activating SOX8 expression.

Project description:In this study, we examined the role of EHMT1 in embryonal rhabdomyosarcoma (ERMS), the most frequent subtype of RMS. We report that EHMT1 plays a key role in the migratory and invasive capacity of ERMS cells in vitro and in vivo. Transcriptomic analysis of EHMT1-depleted cells revealed significant alteration in cell migration and invasion pathways. SOX8, a transcription factor that has key roles in cellular motility was significantly decreased upon EHMT1 loss. Consistently, SOX8 depletion phenotypically mimicked EHMT1 loss. Moreover, RNA-Sequencing of SOX8 depleted cells showed down regulation of several integrin genes. Mechanistically, we show that EHMT1 upregulates SOX8 via regulation of BRD4 expression, and consequently its occupancy at the promoter. Our study reveals a novel EHMT1-SOX8 axis that mediates metastasis in ERMS.

2025-05-16 | GSE274482 | GEO

Extrinsic inflammatory, but not intrinsic oligodendroglial factors contribute to oligodendroglial differentiation block in multiple sclerosis

Project description:Multiple sclerosis (MS) is the most frequent demyelinating disease and despite significant advances in the immunotherapy, disease progression still cannot be prevented. Promotion of remyelination, an endogenous repair process, represents a promising new treatment approach. However, spontaneous remyelination frequently fails in MS lesions due to an impaired differentiation of progenitor cells into mature, myelinating oligodendrocytes. Intrinsic oligodendroglial and extrinsic inflammatory factors may contribute to this differentiation block. Therefore, we compared induced pluripotent stem cell (iPSC)-derived oligodendrocytes (hiOL) from MS patients and healthy controls as well as their response to extrinsic factors. While functional capabilities or proteome compostion of both cell types were virtually indistinguishable, we discovered that Interferon-gamma (IFNÎ³) producing immune cells significantly impaired oligodendroglial differentiation and observed no differences in the functional capabilities or the proteome. In summary, these data indicate that the oligodendroglial differentiation block is not due to intrinsic oligodendroglial factors, but rather caused by the inflammatory environment present in MS lesions. These findings may contribute to the development of remyelination promoting strategies in MS.

2020-09-04 | PXD016043 | Pride

Sox10 is required for systemic initiation of bone mineralization

Project description:Heterozygous variants in SOX10 cause syndromes affecting pigmentation, digestion, hearing, and neural development, primarily attributable to failed differentiation or loss of non-skeletal neural crest derivatives. We report here an additional novel requirement for Sox10 in bone mineralization. Neither crest- nor mesoderm-derived bones initiate mineralization on time in zebrafish sox10 mutants, despite normal osteoblast differentiation and matrix production. Mutants are deficient in the Trpv6+ ionocytes that take up calcium from the environment, resulting in severe calcium deficiency. As these ionocytes derive from ectoderm, not crest, we hypothesized that the primary defect resides in a separate organ that systemically regulates ionocyte numbers. RNAseq revealed significantly elevated stanniocalcin (Stc1a), an anti-hypercalcemic hormone, in sox10 mutants. Stc1a inhibits calcium uptake in fish by repressing trpv6 expression and Trpv6+ ionocyte proliferation. Epistasis assays confirm excess Stc1a as the proximate cause of the calcium deficit. The pronephros-derived glands that synthesize Stc1a interact with sox10+ cells, but these cells are missing in mutants. We conclude that sox10+ crest-derived cells non-autonomously limit Stc1a production to allow the inaugural wave of calcium uptake necessary to initiate bone mineralization.

2025-01-07 | GSE283071 | GEO

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