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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [MeRIP-Seq]

ABSTRACT: Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [MeRIP-Seq]

PROVIDER: PRJNA766593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16082800_1.fastq.gz	Fastqsanger.gz
	SRR16082800_2.fastq.gz	Fastqsanger.gz
	SRR16082801_1.fastq.gz	Fastqsanger.gz
	SRR16082801_2.fastq.gz	Fastqsanger.gz
	SRR16082802_1.fastq.gz	Fastqsanger.gz

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [MeRIP-Seq]

Project description:Improvements in living standards have led to non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases worldwide. Recent studies have shown that N6-methyladenosine (m6A), a type of RNA modification, is strongly associated with many important biological processes. However, the relationship between m6A methylation modifications and NAFLD remains poorly understood. In the present study, through methylated RNA immunoprecipitation sequencing and RNA transcriptome sequencing in high fructose diet-induced NAFLD mice, we found that hypermethylation-encoding genes were mainly enriched in lipid metabolism processes. We identified 266 overlapping and differentially expressed genes (DEGs) that changed at both the mRNA expression level and m6A modification level. Among them, 193 genes displayed increased expression and m6A modification, indicating that m6A RNA modifications tend to be positively correlated with NAFLD. We further compared the high fructose diet-induced NAFLD mouse model with leptin receptor-deficient mice and found that DEGs enriched in the lipid metabolism pathway were up-regulated in both groups. In contrast, DEGs associated with the immune inflammatory response were up-regulated in the high fructose diet group, but down-regulated in leptin receptor-deficient mice. Taken together, our results demonstrate that m6A methylation modifications may play an important role in the development of NAFLD.

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-Seq]

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease

Project description:Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

Project description:Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-Seq]

Project description:Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-Seq]

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Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease.

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Gene expression profiling of fructose and food preservative-induced non-alcoholic fatty liver disease in mice

Project description:This study investigates the synergistic effects of fructose and common food preservatives (sodium benzoate, sodium nitrite, and potassium sorbate) on the development of non-alcoholic fatty liver disease (NAFLD) using a human-microbiota-associated mouse model. We examined changes in hepatic gene expression through microarray analysis to understand the molecular mechanisms underlying NAFLD progression in response to these dietary factors.

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Project description:We show that N6-methyladenosine (m6A), the most abundant internal modification in mRNA/lncRNA with still poorly characterized function, alters RNA structure to facilitate the access of RBM for heterogeneous nuclear ribonucleoprotein C (hnRNP C). We term this mechanism m6A-switch. Through combining PAR-CLIP with Me-RIP, we identify 39,060 m6A-switches among hnRNP C binding sites transcriptome-wide. We show that m6A-methyltransferases METTL3 or METTL14 knockdown decreases hnRNP C binding at 16,582 m6A-switches. Taken together, 2,798 m6A-switches of high confidence are identified to mediate RNA-hnRNP C interactions and affect diverse biological processes including cell cycle regulation. These findings reveal the biological importance of m6A and provide insights into the sophisticated regulation of RNA-RBP interactions through m6A-induced RNA structural remodeling. Measure the m6A methylated hnRNP C binding sites transcriptome-wide by PARCLIP-MeRIP; measure the differential hnRNP C occupancies upon METTL3/METTL14 knockdown by PAR-CLIP; measure RNA abundance and splicing level changes upon HNRNPC, METTL3 and METTL14 knockdown

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