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Effect of Ythdf2 in haematopoiesis [RNA-seq]

ABSTRACT: The mRNA m6A reader YTHDF2 is overexpressed in human acute myeloid leukaemias. To understand the role of YTHDF2 in normal haematopoiesis and ageing, we performed SMART-seq on haematopoietic stem cells (HSCs) derived from young and aged (1 year old) mice. In parallel, to identify transcripts likely methylated in HSCs we performed meRIP-seq analysis of c-Kit+ cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE142019 | GEO | 2020/10/29

REPOSITORIES: GEO

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Effect of Ythdf2 in haematopoiesis [meRIP-seq]

Project description:The mRNA m6A reader YTHDF2 is overexpressed in human acute myeloid leukaemias. To understand the role of YTHDF2 in normal haematopoiesis and ageing, we performed SMART-seq on haematopoietic stem cells (HSCs) derived from young and aged (1 year old) mice. In parallel, to identify transcripts likely methylated in HSCs we performed meRIP-seq analysis of c-Kit+ cells.

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MeRIP, RIP and RNA Sequencing of the H1299 stable cell lines which the endogenous YTHDF2 was silenced by a short hairpin RNA targeting YTHDF2 3’UTR (shYTHDF2) and then re-expressed Flag-tagged YTHDF2-WT orYTHDF2-K571R

Project description:SUMOylation affects many aspects of target proteins such as activity, stability, localization and protein-protein interactions. We have found that SUMOylation of YTHDF2 increased its binding activity with m6A-RNAs by using different experimental approaches. To confiremd this conclusion,the analysis of RIP-seq, MeRIP-seq and RNA-seq in H1299-shYTHDF2 cells re-expressing YTHDF2-WT and YTHDF2-K571R was performed. MeRIP+RIP targets showed lower binding affinities in the mutant YTHDF2-K571R when compared with YTHDF2-WT. Compared to the control group, the binding capacities of YTHDF2 to RIP targets in treated group with either 2-D08 or GA were decreased, especially to MeRIP+RIP targets. Moreover, SUMOylated YTHDF2 promoted m6A-RNAs degradation. Combined analysis of RNA-seq, RIP-seq and MeRIP-seq showed that the mRNA levels were up-regulated in shYTHDF2 stable cells re-expressing YTHDF2-K571R compared with those in re-expressing YTHDF2-WT.

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YTHDF2 iCLIP in glioblastoma stem cells

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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YTHDF2 mediates the mRNA degradation in prostate cancer in m6A-dependent way

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GATA2 mitotic bookmarking is required for definitive haematopoiesis [ChIP-seq]

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