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Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord

ABSTRACT: Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord

PROVIDER: PRJNA679077 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13074806.fastq.gz	Fastqsanger.gz
	SRR13074807.fastq.gz	Fastqsanger.gz
	SRR13074808.fastq.gz	Fastqsanger.gz
	SRR13074809.fastq.gz	Fastqsanger.gz
	SRR13074810.fastq.gz	Fastqsanger.gz

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Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord [transcriptome]

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Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord [transcriptome]

Project description:Spinal cord injury (SCI) results in loss of neurons, oligodendrocytes and myelin sheaths, all of which are not efficiently restored. The scarcity of oligodendrocytes in the lesion site impairs remyelination of spared fibres, which leaves axons denuded, impedes signal transduction and contributes to permanent functional deficits. In contrast to mammals, zebrafish can functionally regenerate the spinal cord. Yet, little is known about oligodendroglial lineage biology and remyelination capacity after SCI in a regeneration-permissive context. Here, we report that in adult zebrafish, SCI results in axonal, oligodendrocyte and myelin sheath loss. We find that OPCs, the oligodendorocyte progenitor cells, survive the injury, enter a reactive state, proliferate and differentiate into oligodendrocytes. Concomitantly, the oligodendrocyte population is re-established to pre-injury levels within two weeks.Transcriptional profiling revealed that reactive OPCs upregulate the expression of several myelination-related genes. Interestingly, global reduction of axonal tracts and partial re-myelination, relative to pre-injury levels, persist at later stages of regeneration, yet suffices for functional recovery. Taken together, these findings imply that in the zebrafish spinal cord, OPCs replace lost oligodendrocytes and, thus, re-establish myelination during regeneration.

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Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord [Single cell]

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Project description:Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord [Single cell]

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Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord

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

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Distinct oligodendrocyte populations have spatial preference and different responses to spinal cord injury

Project description:In this study, we unveil that transcriptionally distinct oligodendrocyte populations have spatial preference and differential response to spinal cord injury. We also assess by different methods, including single-cell RNA sequencing, that the developmental origin of oligodendrocyte progenitors does not determine their specification into mature olgodendrocyte populations.

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Expression data from Sip1 cKO and control mice spinal cord

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/β-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 β-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. We carried out microarray profiling analysis in the Sip1 conditional KO (cKO) mouse spinal cord to detail the change of global gene expression. Sip1 c/c;Olig1-Cre mouse spinal cord was collected at P14 for RNA extraction and Affymetrix microarray analysis. Sip1 c/+;Olig1-Cre littermate spinal cord was used as the control.

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