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Differential effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

ABSTRACT: We developed a method to deconvolute decays of m6A mRNAs and their unmethylated isoforms from total RNAs across the transcriptome and combined it with the knockdown of m6A reader protein to study it's effect on global mRNA turnover.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181814 | GEO | 2025/02/01

REPOSITORIES: GEO

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	GSE181814_Shyu_isoform_TPM_annotation_data.txt.gz	Txt

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Effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

Project description:We developed a method to deconvolute decays of m6A mRNAs and their unmethylated isoforms from total RNAs across the transcriptome and combined this method with the knockdown of m6A reader protein to study the effect on global mRNA turnover.

2025-02-01 | GSE218263 | GEO

Effects of m6A modification on turnover of newly synthesized mRNAs at the transcriptome level.

Project description:We developed a method to deconvolute decays of m6A mRNAs and their unmethylated isoforms from newly synthesized total RNAs across the transcriptome to study the effects of m6A modification on decays of not only the m6A-modified RNA pool but also the unmehnylated isoform pool.

2025-02-01 | GSE218267 | GEO

MOV10 facilitates messenger RNA decay in an N6-methyladenosine (m6A)-dependent manner to maintain the mouse embryonic stem cells state

Project description:N6-methyladenosine (m6A) is the most predominant internal mRNA modification in eukaryotes, recognised by its reader proteins (so-called m6A-readers) for regulating subsequent mRNA fates – splicing, export, localization, decay, stability and translation – to control several biological processes. Although a few m6A-readers have been identified, yet the list is incomplete. Here, we identify a new m6A-reader protein, MOV10, in mouse embryonic stem cells (mESCs). MOV10 recognises m6A-containing mRNAs with a conserved GGm6ACU motif. Mechanistic studies uncover that MOV10 bound m6A-containing mRNAs facilitate mRNA decay within the cytoplasmic processing bodies (P-bodies) in an m6A-dependent manner. Moreover, MOV10 decays the Gsk-3ß mRNA through m6A that stabilises the ß-CATENIN expression of a Wnt/ß-catenin signalling pathway to regulate downstream target expression of NANOG for maintaining the mESC state. Thus, our findings reveal how a newly identified m6A-reader, MOV10 mediates mRNA decay via m6A that impact ESC biology.

2024-01-15 | GSE181821 | GEO

Cell cycle-dependent YTHDF2 promotes mitotic entry by repressing WEE1

Project description:The m6A modification regulates mRNA stability and translation. Here we show that transcriptomic m6A modification is dynamic and the m6A reader protein YTHDF2 promotes mRNA decay during the cell cycle. Depletion of YTHDF2 leads to the delay of mitotic entry due to overaccumulation of WEE1, a negative regulator of CDK1. We demonstrate that WEE1 transcripts contain m6A modification, which promotes their decay through the m6A reader YTHDF2. Moreover, we found that YTHDF2 protein stability is dependent on CDK1 activity. Thus, CDK1, YTHDF2, and WEE1 form a feedforward regulatory loop to promote mitotic entry. We further identified CUL1, CUL4A, DDB1, and SKP2 as components of E3 ubiquitin ligase complexes that mediate YTHDF2 proteolysis. Our study provides insights into how cell cycle mediators modulate transcriptomic m6A modification, which in turn regulates the cell cycle.

2020-01-01 | GSE134700 | GEO

SLAM-Seq analysis of Ythdf2-deficient pre-leukemic cells

Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To study the role of YTHDF2 on mRNA decay rates in leukemia, c-Kit+ cells from foetal livers of Ythdf2fl/fl; Vav-iCre (Ythdf2CKO) and Ythdf2fl/fl (Ythdf2CTL) 14.5 dpc embryos were transduced with Meis1 and Hoxa9 oncogenes and serially re-plated to generate pre-leukemic cells. Medium with 4SU was used for pre-leukemic cells labelling for 12 hours and was later replaced with 4SU-free medium (time 0). Cells were collected immediately after medium change and at 1, 3 and 9 hours for library generation. RNA from Ythdf2CKO (n=3 biological replicates) and Ythdf2CTL (n=3 biological replicates) pre-leukemic cells were used for SLAM-seq library generation.

2019-04-05 | E-MTAB-7784 | biostudies-arrayexpress

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

Project description:As the crucial m6A reader, YTHDF2 usually degrades the target mRNAs by recognizing the m6A modified sites, consequently altering m6A levels of each mRNA. In this study, we used m6A MeRIP sequencing to detect the m6A modification alterations in prostate cancer (PCa) cell line after knocking down YTHDF2 and identify how YTHDF2 promote the PCa progression by mediating the mRNA degradation in m6A-dependent way.

2020-11-09 | GSE129408 | GEO

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.

2020-09-29 | GSE158020 | GEO

Structural basis of YTH domain as m6A reader

Project description:The N6-methyladenosine (m6A) is the most abundant internal modification in almost all eukaryotic messenger RNAs, and is dynamically regulated. Therefore, identification of m6A readers is especially important in determining the cellular function of m6A. YTHDF2 has recently been characterized as the first m6A reader that regulates the cytoplasmic stability of methylated RNA. Here we show that YTHDC1 is a nuclear m6A reader and report the crystal structure of the YTH domain of YTHDC1 bound to m6A-containing RNA. We further determined the structure of another YTH domain, YTHDF1, and found that the YTH domain utilizes a conserved aromatic cage to specifically recognize the methyl group of m6A. Our structural characterizations of the YTHDC1-m6A RNA complex also shed light on the molecular basis for the preferential binding of the GG(m6A)C sequence by YTHDC1 and confirm the YTH domain as a specific m6A RNA reader. PAR-CLIP (Photoactivatable-Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) was applied to human YTHDC1 protein to identify its binding sites.

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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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Effect of Ythdf2 in haematopoiesis [RNA-seq]

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