Global analysis of m6A mRNA methylation in human cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA695454 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13570924.fastq.gz | Fastqsanger.gz | |||
| SRR13570925.fastq.gz | Fastqsanger.gz | |||
| SRR13570926.fastq.gz | Fastqsanger.gz | |||
| SRR13570927.fastq.gz | Fastqsanger.gz | |||
| SRR13570928.fastq.gz | Fastqsanger.gz |
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Project description:N6-methyladenosine (m6A) is the most abundant internal modification on mRNA which influences most steps of mRNA metabolism and is involved in several biological functions. The E3 ubiquitin ligase Hakai was previously found in complex with components of the m6A methylation machinery in plants and mammalian cells but its precise function remained to be investigated. Here we show that Hakai is a conserved component of the methyltransferase complex in Drosophila and human cells. In Drosophila, its depletion results in reduced m6A levels and altered m6A-dependent functions including sex determination. We show that its ubiquitination domain is required for dimerisation and interaction with other members of the m6A machinery, while its catalytic activity is dispensable. Finally, we demonstrate that the loss of Hakai destabilizes several subunits of the methyltransferase complex, resulting in impaired m6A deposition. Our work adds new functional and molecular insights into the mechanism of the m6A mRNA writer complex.
2021-04-29 | PXD022294 | Pride
Project description:m6A RNA immunoprecipitation was performed according to published procedure (Dominissini et al., 2012). Human m6A-seq data from DTSC2 HeLa cells were aligned to the hg19 transcriptome. To locate m6A peaks, the hg19 transcriptome was divided into 25 nucleotide-wide tiles. The number of reads in the m6A immunoprecipitation (IP) and non-IP (control) sample was counted in each tile, and a p-value was calculated using Fisher’s exact test and adjusted for multiple testing. Tiles with significant enrichment of the m6A signal (adjust-P value < = 0.05) were merged into larger regions. Regions lesser than 100 bp were discarded, and regions over 200 bp were separated into 100 to 200 bp sub-regions; the m6A signal from rapamycin-treated cells compared to control (DMSO) was calculated for each region; and regions with at least a two-fold enrichment in all replicates were identified as m6A peaks. The distributions of m6A peaks and m6A marked genes were identified by overlapping all m6A peaks with the hg19 RefGene annotation (Meng et al., 2014).
2021-02-17 | GSE165690 | GEO
Project description:N6-methyladenosine (m6A) RNA methylation is the most abundant internal chemical modifications in eukaryotic messenger RNA (mRNA) as well as long non-coding RNA (lncRNA). Recently, m6A RNA methylation research was revived by the discovery of the fat mass- and obesity-associated protein (FTO) as the first RNA demethylase, implicating that m6A RNA methylation is a reversible and dynamic modification and may have critical biological functions. Emerging evidence has shown that m6A modifications in mRNAs and lncRNAs play crucial roles in regulating RNA fate and function in biological processes in the past several years. The goal is to determine the targets of arsenic damage including m6A RNA methylation in keratinocytes.
2021-03-01 | GSE145923 | GEO
Project description:Human neurodevelopment requires differentiating neurons to establish large networks of connections in a highly stereotyped manner. Neuronal differentiation in particular, requires RNA-binding proteins to spatiotemporally regulate thousands of different mRNAs. Yet, how these proteins precisely relate to neuronal development and coordinate the expression of functionally coherent genes in a cell type specific manner is only partially understood. To address this, we sought to understand how the paradigmatic RNA-binding protein IMP1/IGF2BP1, an essential developmental factor, selects and regulates its RNA targets transcriptome-wide during the differentiation of human neurons. We used a combination of systemic and molecular analyses to show that IMP1 directly binds to and regulates the expression of a large set of mRNAs that govern microtubule assembly, an essential process and a key driver of neuronal differentiation. We also show that m6A methylation during the transition from neural precursors to neurons drives both the selection of IMP1 mRNA targets and their translation potential. Our findings establish m6A methylation as a key mechanism coordinating the regulatory action of IMP1 on human neuronal architecture.
2024-06-10 | PXD034341 | Pride
Project description:m6A IP sequencing analysis of m6A mRNA methylation regulation by arsenic in keratinocytes
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Project description:m6A IP sequencing analysis of m6A mRNA methylation regulation by YTHDF2 in keratinocytes
| PRJNA608743 | ENA
Project description:Circadian transcriptional rhythms are necessary for lipid metabolic homeostasis. Disruptions can lead to metabolic diseases. Whether epigenetic N6-methyladenosine (m6A) mRNA methylation impacts circadian regulation of lipid metabolism is unclear. Here, we show m6A mRNA methylation oscillations in murine liver depend upon a functional circadian clock. Hepatic deletion of Bmal1 increased m6A mRNA methylation, particularly of PPaRα. Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreased PPaRα m6A abundance and increased PPaRα mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. Our data suggest YTH domain family 2 (YTHDF2, a m6A binding protein) binds to PPaRα, prolonging its lifetime and mRNA expression. Reactive oxygen species accumulation increased PPaRα transcript m6A levels, revealing a possible mechanism for circadian clock disruption on m6A mRNA methylation. These data suggest m6A RNA methylation is important for circadian clock regulation of downstream genes and lipid metabolism that impacts metabolic outcome.
2018-06-21 | GSE102620 | GEO
Project description:m6A is a ubiquitous RNA modification in eukaryotes. Transcriptome-wide m6A patterns in Arabidopsis have been assayed recently. However, m6A differential patterns among organs have not been well characterized. The goal of the study is to comprehensively analyze m6A patterns of numerous types of RNAs, the relationship between transcript level and m6A methylation extent, and m6A differential patterns among organs in Arabidopsis. In total, 18 libraries were sequneced. For the 3 organs: leaf, flower and root, each organ has mRNA-Seq, m6A-Seq and Input sequenced. And each sequence has 2 replicats.
2015-10-28 | E-GEOD-72706 | biostudies-arrayexpress
Project description:N6-methyladenosine (m6A) RNA methylation is the most abundant internal chemical modifications in eukaryotic messenger RNA (mRNA) as well as long non-coding RNA (lncRNA). Recently, m6A RNA methylation research was revived by the discovery of the fat mass- and obesity-associated protein (FTO) as the first RNA demethylase, implicating that m6A RNA methylation is a reversible and dynamic modification and may have critical biological functions. Emerging evidence has shown that m6A modifications in mRNAs and lncRNAs play crucial roles in regulating RNA fate and function in biological processes in the past several years. As the first identified RNA demethylase that regulates the demethylation of target mRNAs, FTO has been reported to play an oncogenic role in leukemia and glioblastoma stem cells. To identify the target genes of FTO in melanoma cells, we used m6A IP seq coupled with RNA seq to determine the potential demethylation and gene targets across the whole transcriptome for FTO, and identified more than 1,000 genes.
2019-05-06 | GSE112902 | GEO
Project description:Circadian transcriptional rhythms are necessary for lipid metabolic homeostasis. Disruptions can lead to metabolic diseases. Whether epigenetic N6-methyladenosine (m6A) mRNA methylation impacts circadian regulation of lipid metabolism is unclear. Here, we show m6A mRNA methylation oscillations in murine liver depend upon a functional circadian clock. Hepatic deletion of Bmal1 increased m6A mRNA methylation, particularly of PPaRα. Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreased PPaRα m6A abundance and increased PPaRα mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. Our data suggest YTH domain family 2 (YTHDF2, a m6A binding protein) binds to PPaRα, prolonging its lifetime and mRNA expression. Reactive oxygen species accumulation increased PPaRα transcript m6A levels, revealing a possible mechanism for circadian clock disruption on m6A mRNA methylation. These data suggest m6A RNA methylation is important for circadian clock regulation of downstream genes and lipid metabolism that impacts metabolic outcome.
2018-10-25 | GSE102619 | GEO