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Analysis of m6A methylome in ABRO1 Knockout heart

ABSTRACT: Analysis of m6A methylome in ABRO1 Knockout heart

PROVIDER: PRJNA779256 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16902529_1.fastq.gz	Fastqsanger.gz
	SRR16902529_2.fastq.gz	Fastqsanger.gz
	SRR16902530_1.fastq.gz	Fastqsanger.gz
	SRR16902530_2.fastq.gz	Fastqsanger.gz
	SRR16902531_1.fastq.gz	Fastqsanger.gz

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Analysis of m6A methylome in ABRO1 Knockout heart

Project description:To find the m6A methylation targets of ABRO1, we performed m6A methylated RNA immunoprecipitation sequencing (MeRIP-seq) in ABRO1 Knockout or Wild type (WT) mice heart. The analysis of the distribution of m6A peak density in mRNA transcripts showed that m6A peaks are mainly found in coding sequences (CDS) and a considerable amount of m6A peaks enriched around start codon and stop codon regions in mRNA transcripts from ABRO1 KO and WT hearts. Among the total RNA transcripts with m6A sites, more than half (59.4%) of mRNA transcripts contain ≤ 2 m6A peaks, 27.4% mRNA transcripts comprise 3 to 5 m6A peaks and more than 5 m6A peaks exist in 13.2% of mRNA transcripts. MeRIP-seq analysis results from ABRO1 deleted hearts showed that a total of 3444 m6A peaks were upregulated and 4631 m6A were downregulated compared to WT hearts.

2023-12-01 | GSE188518 | GEO

Analysis of m6A methylome in CHAPIR overexpressed heart [MeRIP]

Project description:Analysis of m6A methylome in CHAPIR overexpressed heart [MeRIP]

| PRJNA647217 | ENA

Analysis of m6A methylome in CHAPIR overexpressed heart [MeRIP]

Project description:To elucidate the molecular mechanism by which cardiac-hypertrophy-associated piRNA (CHAPIR) regulates m6A modification, we performed m6A methylated RNA immunoprecipitation sequencing (MeRIP-seq) in control or CHAPIR-overexpressing mice heart. The sequential analysis of m6A peaks showed that RGACH motif was highly enriched within m6A sites in heart and that is aligning with the classical consensus sequence of mammals ‘RGACH’, where ‘R’ indicates purine (A/G) and ‘H’ indicates non-guanine base (A/C/U). In CHAPIR treated heart, m6A mostly occurred in mRNAs (89.5%) and only about 10.5% were identified in non-coding RNAs. The majority of mRNAs contain one or two m6A peaks (89.2%) and 10.8% mRNA contain >2 m6A peaks . M6A peaks were predominantly distributed in coding sequences (CDSs), 3’ untranslated regions (3’UTRs) and near stop codon.

2020-07-24 | GSE154699 | GEO

Comprehensive analysis of the transcriptome-wide m6A methylome of neonatal heart regeneration via MeRIP sequencing

Project description:Comprehensive analysis of the transcriptome-wide m6A methylome of neonatal heart regeneration via MeRIP sequencing

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Comprehensive analysis of the transcriptome-wide m6A methylome of neonatal heart regeneration via MeRIP sequencing

Project description:Aim: To systematically classify the profile of the RNA m6A modification landscape of neonatal heart regeneration. Materials and Methods: Cardiomyocyte proliferation markers were detected via immunostaining. The expression of m6A modification regulators was detected using quantitative real-time PCR (qPCR) and Western blotting. Genome-wide profiling of m6A-modified transcripts was conducted with m6A-modified RNA immunoprecipitation sequencing (m6A-RIP-seq) and RNA sequencing (RNA-seq). The Gene Expression Omnibus database (GEO) dataset was used to verify the hub genes. Results: METTL3 and the level of m6A modification in total RNA were lower in P7 rat hearts than in P0 ones. In all, 1637 m6A peaks were differentially expressed using m6A-RIP-seq, with 84 upregulated and 1553 downregulated. Furthermore, conjoint analyses of m6A-RIP-seq, RNA-seq, and GEO data generated eight potential hub genes with differentially expressed hypermethylated or hypomethylated m6A levels. Conclusion: Our data show novel information on m6A modification changes in cardiac regeneration. The modifications made possible by directly modulating m6A may attract future study of cardiac regeneration.

2021-03-31 | GSE162545 | GEO

m6A methylome in JQ1 treatment and control in MDA-MB-231 cells.

Project description:We report the application of MeRIP sequencing technology for high-throughput profiling of m6A methylome in breast cancer cells. Comparison of m6A methylome between control and BETi-treated cells revealed the following findings: 1) Significant global alteration of methylation sites due to BETi-treatment (herein defined as BETi-m6A signature). 2) Gene Ontology (GO) analysis of the differential meRIP-seq candidates enriched pathways involved in chromatin modification, RNA splicing and pathways regulating cell fate , reflecting a critical role of m6A in diverse biological processes.

2023-12-31 | GSE219190 | GEO

HIV-1 m6A methylome investigation by m6A-SAC-seq

Project description:HIV-1 m6A methylome investigation by m6A-SAC-seq

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RNA m6A methylome of Caenorhabditis elegans

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m6A-Label-seq directly reports m6A methylome at base resolution

Project description:m6A-Label-seq directly reports m6A methylome at base resolution

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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

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