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Ythdf2-mediated m6A mRNA clearance modulates neural development in mice

ABSTRACT: Ythdf2-mediated m6A mRNA clearance modulates neural development in mice

PROVIDER: PRJNA414058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6163660.fastq.gz	Fastqsanger.gz
	SRR6163661.fastq.gz	Fastqsanger.gz
	SRR6163662.fastq.gz	Fastqsanger.gz
	SRR6163663.fastq.gz	Fastqsanger.gz
	SRR6163664.fastq.gz	Fastqsanger.gz

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Ythdf2-mediated m6A mRNA clearance modulates neural development in mice

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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The functions of m6A and Ythdf2 during zebrafish early development

Project description:We report the m6A methylation maps of zebrafish embryos during early development, and transcriptome-wide changes occured in ythdf2 LOF mutant embryos. Our study reveals the m6A-dependent RNA decay as a previously unidentified maternal mode mechanism to regulate maternal mRNA clearance during zebrafish MZT, highlighting the critical role of the m6A mRNA methylation in animal development.

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The RNA m6A reader YTHDF2 maintains oncogene expression and is a targetable dependency in glioblastoma stem cells [m6A RIP-seq]

Project description:Glioblastoma is a universally lethal cancer driven by glioblastoma stem cells (GSCs). Here, we interrogated N6-methyladenosine (m6A) mRNA modifications in GSCs by methyl RNA-immunoprecipitation followed by sequencing (meRIP-seq) and transcriptome analysis, finding transcripts marked by m6A often upregulated. Interrogating m6A regulators, GSCs displayed preferential expression as well as in vitro and in vivo dependency of the m6A reader, YTHDF2, in contrast to normal neural stem cells (NSCs). While YTHDF2 has been reported to destabilize mRNAs, YTHDF2 stabilized the oncogene transcripts, MYC and VEGFA, in GSCs in an m6A-dependent manner. We identified IGFBP3 as a downstream effector of the YTHDF2-MYC axis in GSCs and IGF1/IGF1R inhibitor, Linsitinib, as preferentially targeting YTHDF2-expressing cells, inhibiting the viability of GSCs without affecting NSCs and impairing in vivo glioblastoma growth. Thus, YTHDF2 links RNA epitranscriptomic modifications and GSC growth, laying the foundation for the YTHDF2-MYC-IGFBP3 axis as a specific and novel therapeutic target in glioblastoma.

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Stem cells utilize m6A-mediated decay via YTHDF2 to regulate neural differentiation and promote pluripotency

Project description:The m6A methylation pathway has previously been shown to influence pluripotency. YTHDF2 is an RNA binding protein that interacts with m6A-modified RNAs to facilitate their degradation. We sought to identify the cohort of RNAs targeted by YTHDF2 in human induced pluripotent stem cells (iPSC).

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Project description:N6-methyladenosine (m6A) is the most prevalent internal modification present in the mRNA of all higher eukaryotes. Here we present that m6A is selectively recognized by human YTH domain family (YTHDF2) protein to regulate mRNA degradation. By using crosslinking and immunoprecipitation, we have identified over 4000 substrate RNA of YTHDF2 with conserved core motif of G(m6A)C. We further estabilshed the role of YTHDF2 in RNA metabolism by a combination of ribosome profiling, RNA sequencing, m6A level quantification and cell-based imaging: the C-terminal domain of YTHDF2 selectively binds to m6A of mRNA and the N-terminal domain is responsive for localizing mRNA from translatable pool to processing body where mRNA decay occurs. PAR-CLIP and RIP was used to identify YTHDF2 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF2 siRNA knock-down

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