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Changes in m6A RNA methylation contribute to heart failure progression by modulating translation

ABSTRACT: Changes in m6A RNA methylation contribute to heart failure progression by modulating translation

PROVIDER: PRJNA543140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9063780.fastq.gz	Fastqsanger.gz
	SRR9063790.fastq.gz	Fastqsanger.gz
	SRR9063800.fastq.gz	Fastqsanger.gz
	SRR9063810.fastq.gz	Fastqsanger.gz
	SRR9063820.fastq.gz	Fastqsanger.gz

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Changes in m6A RNA methylation contribute to heart failure progression by modulating translation

Project description:We analysed m6A RNA methylation via next generation sequencing (NGS). We found that approximately one quarter of the transcripts in the healthy mouse and human heart exhibit m6A RNA-methylation. There was a mild positive correlation of m6A RNA-methylation at the 5’UTR and coding region with transcript level while m6A RNA-methylation at the 3’UTR showed a mild negative correlation. When we analyzed heart failure in mice and humans we observed that changes in m6A RNA-methylation exceed changes in gene-expression. In mouse and human heart failure transcripts with altered m6A RNA-methylation were mainly linked to metabolic and regulatory pathways while changes in transcript level mainly represented changes in structural plasticity. Mechanistically we could link m6A RNA-methylation to altered RNA translation and protein production. Furthermore, mice with a cardiomyocyte restricted knockout of the demethylase Fto show an impaired function compared to control mice. Thus, we describe for the first time m6A RNA methylation at the genome-wide level in the human heart and in addition use mouse models to provide evidence that changes in m6A RNA-methylation play an important role in heart failure development by affecting regulatory pathways distinct from those genes with altered expression levels regulate. Our data suggest that modulation of epitranscriptomic processes such as m6A-methylation might be an interesting target for therapeutic interventions.

2019-05-16 | GSE131296 | GEO

m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation

Project description:In summary, we characterized the role of m6A modification in pulmonary fibrosis. We reveal that m6A modification is increased in bleomycin induced pulmonary fibrosis mice model, FMT-derived myofibroblasts and idiopathic pulmonary fibrosis patient lung samples. Lowering m6A level through silencing METTL3 suppress FMT process in vitro and vivo. Fundamentally, m6A modification regulates FMT by modulating the translation of KCNH6 mRNA in a YTHDF1 dependent manner. This study provides novel insights into the mechanism of FMT process and suggests m6A modification intervention may be a promising therapeutic strategy for pulmonary fibrosis.

2021-06-02 | GSE164151 | GEO

m6A in 5â untranslated regions promotes cap-independent translation of mRNA

Project description:N6-methyladenosine (m6A) is a widespread internal RNA modification whose function is poorly understood. Here we report that m6A residues within the 5'UTR promote a novel form of cap-independent translation which is mediated through an interaction between m6A residues and the translation initiation factor, eIF3. We present eIF3a PAR-iCLIP data which demonstrate that eIF3 predominantly binds mRNAs within the 5'UTR. eIF3 binding sites are also in proximity to m6A residues within the 5'UTR of cellular mRNAs. Two replicates of eIF3a PAR-iCLIP in HEK293T cells.

2015-10-26 | E-GEOD-73405 | biostudies-arrayexpress

m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation

Project description:m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation

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MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

Project description:MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

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N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress

m6A in 5’ untranslated regions promotes cap-independent translation of mRNA

Project description:N6-methyladenosine (m6A) is a widespread internal RNA modification whose function is poorly understood. Here we report that m6A residues within the 5'UTR promote a novel form of cap-independent translation which is mediated through an interaction between m6A residues and the translation initiation factor, eIF3. We performed m6A profiling in cells subjected to heat shock stress and observed increased 5'UTR methylation after heat shock. For these studies, we used single-nucleotide resolution m6A mapping (miCLIP), which enables the detection of m6A residues separately from m6Am residues. Thus, the goal of these experiments was to identify m6A residues which are increased in the 5'UTR after heat shock stress.

2015-10-26 | GSE73405 | GEO

Crosstalk between EZH2 and m6A RNA methylation promotes prostate cancer progression through modulating an m6A autoregulation pathway

Project description:N6-methyladenosine (m6A), the most predominant RNA modification in humans, participates in various fundamental and pathological bioprocesses. Dynamic manipulation of m6A deposition in the transcriptome is critical for cancer progression, while how this regulation is achieved remains understudied. Here, we report that in prostate cancer (PCa), Polycomb group (PcG) protein Enhancer of Zeste Homolog 2 (EZH2) exerts an additional function in m6A regulation via its enzymatic activity. Mechanistically, EZH2 methylates and stabilizes FOXA1 proteins from degradation, which in turn facilitates the transcription of m6A reader YTHDF1. Through activating a m6A autoregulation pathway, YTHDF1 enhances the translation of METTL14 and WTAP, two critical components of the m6A methyltransferase complex (MTC), and thereby upregulates the global m6A level in PCa cells. We further demonstrate that inhibiting the catalytic activity of EZH2 suppresses the translation process globally through targeting the YTHDF1-m6A axis. By disrupting both the expression and interaction of key m6A MTC subunits, combinational treatment of EZH2 degrader MS8815 and m6A inhibitor STM2457 mitigates PCa tumor growth synergistically. Together, our study decodes a previously hidden interrelationship between EZH2 and RNA modification, which may be leveraged to advance the EZH2-targeting curative strategies in cancer.

2025-10-05 | GSE296858 | GEO

m6A RNA Methylation Is Regulated by MicroRNAs and Promotes Reprogramming to Pluripotency

Project description:N6-methyladenosine (m6A) has been recently identified as a conserved epitranscriptomic modification of eukaryotic mRNAs, but its features, regulatory mechanisms, and functions in cell reprogramming are largely unknown. Here, we report m6A modification profiles in the mRNA transcriptomes of four cell types with different degrees of pluripotency. Comparative analysis reveals several features of m6A, especially gene- and cell-type-specific m6A mRNA modifications. We also show that microRNAs (miRNAs) regulate m6A modification via a sequence pairing mechanism. Manipulation of miRNA expression or sequences alters m6A modification levels through modulating the binding of METTL3 methyltransferase to mRNAs containing miRNA targeting sites. Increased m6A abundance promotes the reprogramming of mouse embryonic fibroblasts (MEFs) to pluripotent stem cells; conversely, reduced m6A levels impede reprogramming. Our results therefore uncover a role for miRNAs in regulating m6A formation of mRNAs and provide a foundation for future functional studies of m6A modification in cell reprogramming. m6A-seq in ESC, iPSC, NSC and sertoli cells.

2015-03-10 | E-GEOD-52125 | biostudies-arrayexpress

MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

Project description:N6-Methyladenosine (m6A) is the most prevalent internal modification in mammalian mRNAs, and participates in various fundamental bioprocesses as well as cancer. Here we immunoprecipitated m6A methylated poly (A+) RNAs (MeRIP) and then sequenced and profiled mRNA m6A methylation in P493-6 cells.

2020-12-18 | GSE150892 | GEO

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