Correlations of m6A Methylation-Related mRNAs with Thyroid Cancer
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PROVIDER: PRJNA1212738 | ENA |
REPOSITORIES: ENA
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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.
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Project description:N6-methyladenosine (m6A) is the most abundant modified base in eukaryotic mRNA and has been linked to diverse effects on mRNA fate and function. Current m6A mapping approaches rely on immunoprecipitation of m6A-containing RNA fragments to identify regions of transcripts that contain m6A. This approach localizes m6A residues to 100-200 nt-long regions of transcripts. The precise position of m6A in mRNAs cannot be identified on a transcriptome-wide level because there are no chemical methods to distinguish between m6A and adenosine. Here we show that anti-m6A antibodies can induce specific mutational signatures at m6A residues after ultraviolet light-induced antibody-RNA crosslinking and reverse transcription. Similarly, we find these antibodies induce mutational signatures at N6, 2’-O-dimethyladenosine (m6Am), a nucleotide found at the first encoded position of certain mRNAs. Using these mutational signatures, we map m6A and m6Am at single-nucleotide resolution in human and mouse mRNA and identify snoRNAs as a novel class of m6A-containing ncRNAs. UV-crosslinking and immunoprecipitation with m6A-specific antibodies was used to map m6A and m6Am in cellular RNA with single nucleotide resolution.
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Project description:Abstract Background: Cerebral ischemia-reperfusion (I/R) frequently caused the late-onset neuronal damage. Breviscapine has a promote in autophagy of microvascular endothelial cells in I/R and it can inhibit the oxidative damage and apoptosis. However, the mediation mechanism of breviscapine on neuronal cell death is unclear. Methods: Firstly, transcriptome sequencing was performed on three groups of mice neuronal normal group (Control group), oxygen-glucose deprivation/reoxygenation group (OGD/R group) and breviscapine administration group (Therapy group). Differentially expressed genes (DEGs) between OGD/R and Control groups, and between Therapy and OGD/R groups were obtained by limma package. The N6-methyladenosine (m6A) methylation related DEGs were selected out by the Pearson correlation analysis. Then, prediction and confirmation of drug targets were performed by Swiss Target Prediction and UniProt Knowledgebase (UniProtKB) datebase, and key genes were obtained by Pearson correlation analysis between m6A-related DEGs and drug target genes. Next, gene set enrichment (GSEA) analysis and Ingenuity pathway analysis (IPA) were used to obtain the pathways of key genes. Finally, a circRNA-miRNA-mRNA network was constructed based on the mRNAs, circRNAs and miRNAs. Results: 2250 DEGs between OGD/R and Control groups and 757 DEGs between Therapy and OGD/R groups were selected out by differential analysis. A total of 7 m6A related DEGs including Arl4d, Gm10653, Gm1113, Kcns3, Olfml2a, Stk26 and Tfcp2l1 were obtained by Pearson correlation analysis. Four key genes (Tfcp2l1, Kcns3, Olfml2a and Arl4d) were acquired, and GSEA showed that these key genes were significantly participated in DNA repair, e2f targets and g2m checkpoint. IPA revealed that Tfcp2l1 played a significant role in human embryonic stem cell pluripotency. The circRNA-miRNA-mRNA network showed that the mmu_circ_0001258 regulated the Tfcp2l1 by mmu-miR-301b-3p. Conclusions: In conclusion, four key genes including Tfcp2l1, Kcns3, Olfml2a and Arl4d significantly associated with the treatment of OGD/R by breviscapine were acquired, which would provide a theoretical basis for clinical trials.
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