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M6A mRNA methylation is essential for oligodendrocyte maturation and CNS myelination

ABSTRACT: m6A mRNA methylation is essential for oligodendrocyte maturation and CNS myelination

PROVIDER: PRJNA562595 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10028100.fastq.gz	Fastqsanger.gz
	SRR10028101.fastq.gz	Fastqsanger.gz
	SRR10028102.fastq.gz	Fastqsanger.gz
	SRR10028103.fastq.gz	Fastqsanger.gz
	SRR10028104.fastq.gz	Fastqsanger.gz

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m6A mRNA methylation is essential for oligodendrocyte maturation and CNS myelination

Project description:Oligodendrocytes are responsible for myelin formation and axonal trophic support in the vertebrate CNS. While a number of factors have been discovered that regulate oligodendrocyte lineage progression, the exact molecular mechanisms involved in this process remain unclear. Emerging studies have shown that N6-methyladenosine (m6A), the most common internal RNA modification of mammalian mRNA, plays a critical role in various developmental processes. In this study, we demonstrate that oligodendrocyte lineage progression is accompanied by changes in m6A modification on numerous transcripts. In vivo conditional inactivation in oligodendrocyte lineage cells of an essential m6A writer component, METTL14, results in decreased oligodendrocyte numbers and CNS hypomyelination, although oligodendrocyte precursor cell (OPC) numbers are normal. In vitro Mettl14 ablation disrupts post-mitotic oligodendrocyte maturation. In addition, Mettl14 ablation has distinct effects on OPC and oligodendrocyte transcriptomes. Together, our findings indicate that dynamic RNA methylation plays a critical regulatory role in oligodendrocyte development and CNS myelination.

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Project description:Long noncoding RNAs (lncRNAs) are emerging as important regulators of cellular functions, but their roles in myelination in the CNS remain undefined. Through de novo transcriptome reconstruction at multiple stages, we establish dynamic expression profiles of lncRNAs during oligodendrocyte lineage progression and uncover a cohort of oligodendrocyte-enriched lncRNAs. Co-expression network analysis reveals a cohort of lncRNAs is linked to protein-coding genes associated with oligodendrocyte maturation. We identify a conserved chromatin-associated oligodendrocyte-restricted lncRNA, lncOL1. Overexpression of lncOL1 promotes oligodendrocyte differentiation in the developing brain, whereas genetic inactivation of lncOL1 causes defects in myelination and remyelination in the CNS. We further show that lncOL1 interacts with Suz12, a component of polycomb repressive complex 2, to promote oligodendrocyte differentiation in part through Suz12-mediated silencing of a differentiation inhibitory network that antagonizes OL maturation. Together, our findings demonstrate lncRNAs as a key layer of the genetic circuitry that controls CNS myelination and myelin repair.

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