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N6-methyladenosine (m6A) profiling of type II diabetes islets

ABSTRACT: N6-methyladenosine (m6A) profiling of type II diabetes islets

PROVIDER: PRJNA491415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7851600.fastq.gz	Fastqsanger.gz
	SRR7851610.fastq.gz	Fastqsanger.gz
	SRR7851620.fastq.gz	Fastqsanger.gz
	SRR7851591.fastq.gz	Fastqsanger.gz
	SRR7851601.fastq.gz	Fastqsanger.gz

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N6-methyladenosine (m6A) profiling of type II diabetes islets

Project description:In type 2 diabetes, pancreatic beta-cells fail to compensate for the presence of insulin resistance in target tissues and represent a central player in the disease development. Identifying and studying innovative molecular mechanisms that lead to beta-cell failure in diabetes represent an interesting line of research and are necessary. N6-Methyladenosine (m6A) is the most abundant modification in mRNA and is found virtually in all mammals. Through m6A-profiling, we aim to characterize the dynamic RNA methylation changes in islets obtained from patients with type 2 diabetes.

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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

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YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

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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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