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ABSTRACT: Differentiation of NSPCs to Differentiated Neural Progeny

PROVIDER: PRJNA531489 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8866520_1.fastq.gz	Fastqsanger.gz
	SRR8866520_2.fastq.gz	Fastqsanger.gz
	SRR8866521_1.fastq.gz	Fastqsanger.gz
	SRR8866521_2.fastq.gz	Fastqsanger.gz
	SRR8866522_1.fastq.gz	Fastqsanger.gz

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Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L

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Project description:We found that the proliferation and differentiation capabilities of NSPCs decrease significantly in Ythdf2 null mutants.To explore the underlying molecular mechanism, we performed transcriptomics and well-established m6A-methylome analyses of NSPCs dervied from wild type and Ythdf2-/- embryo brains. RNA-seq data revealed that expressions of genes enriched in neural development pathways were significantly disturbed. The inhibitory genes, like Flrt2, Ptprd, et al. in regulation of JAK-STAT cascade, which contributes to the neuroprotection and neurite outgrowth, showed increased gene expressions and m6A enrichment by m6A-seq. We identified that without the recognizing and binding of Ythdf2, the degradation of neuron differentiation related m6A-modified mRNAs were delayed in Ythdf2-/-, thereby disturbing the proliferation and differentiation of NSPCs. In summary, our findings uncovered that Ythdf2 modulates neural developmental via regulating the clearance of mRNA targets.

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