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Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation

ABSTRACT: Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation

PROVIDER: PRJNA839367 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19268400_1.fastq.gz	Fastqsanger.gz
	SRR19268400_2.fastq.gz	Fastqsanger.gz
	SRR19268101_1.fastq.gz	Fastqsanger.gz
	SRR19268101_2.fastq.gz	Fastqsanger.gz
	SRR19268401_1.fastq.gz	Fastqsanger.gz

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Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation [ChIP-seq]

Project description:Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation [ChIP-seq]

| PRJNA839372 | ENA

Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation [RNA-seq]

Project description:Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation [RNA-seq]

| PRJNA839371 | ENA

Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation [RNA-seq]

Project description:The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves largescale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-b1, a key mediator of survival at this transient stage. Constitutive Tns3 loss-of-function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of Tns3 in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a two-fold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-b1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.

2022-09-01 | GSE203294 | GEO

Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation [ChIP-seq]

2022-09-01 | GSE203293 | GEO

Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation.

Project description:The differentiation of oligodendroglia from oligodendrocyte precursor cells (OPCs) to complex and extensive myelinating oligodendrocytes (OLs) is a multistep process that involves large-scale morphological changes with significant strain on the cytoskeleton. While key chromatin and transcriptional regulators of differentiation have been identified, their target genes responsible for the morphological changes occurring during OL myelination are still largely unknown. Here, we show that the regulator of focal adhesion, Tensin3 (Tns3), is a direct target gene of Olig2, Chd7, and Chd8, transcriptional regulators of OL differentiation. Tns3 is transiently upregulated and localized to cell processes of immature OLs, together with integrin-β1, a key mediator of survival at this transient stage. Constitutive <i>Tns3</i> loss of function leads to reduced viability in mouse and humans, with surviving knockout mice still expressing Tns3 in oligodendroglia. Acute deletion of <i>Tns3</i> in vivo, either in postnatal neural stem cells (NSCs) or in OPCs, leads to a twofold reduction in OL numbers. We find that the transient upregulation of Tns3 is required to protect differentiating OPCs and immature OLs from cell death by preventing the upregulation of p53, a key regulator of apoptosis. Altogether, our findings reveal a specific time window during which transcriptional upregulation of Tns3 in immature OLs is required for OL differentiation likely by mediating integrin-β1 survival signaling to the actin cytoskeleton as OL undergo the large morphological changes required for their terminal differentiation.

| S-EPMC9596163 | biostudies-literature

Focal Adhesion Kinase Dependent Expression

Project description:The goal of this study was to identify transcripts, which are differentially regulatulated in the presence and absence of Focal Adhesion Kinase. As Focal Adhesion Kinase activity can depend upon cell density (Snijder et al. Nature 2009), biological replicates where cells, were seeded very sparsely or confluently, were used. Focal Adhesion Kinase Knockout (ATCC CRL-2644) and Rescue Cells (Sieg et al. 1998, clone DA2) were seeded at two different concentrations. Replicas refer to biological replicates, performed on different days. Only one single technical replicate has been done per biological replicate.

2013-09-17 | E-GEOD-43873 | biostudies-arrayexpress

Focal Adhesion Kinase Dependent Expression

2013-09-17 | GSE43873 | GEO

Transient regulation of focal adhesion via Tensin3 is required for nascent oligodendrocyte differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-01 | GSE203295 | GEO