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Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer

ABSTRACT: To investigate the targets of METTL16-induced m6A modification, we established AGS lines in which METTL16 has been knocked down by shRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE224890 | GEO | 2023/10/05

REPOSITORIES: GEO

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Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer

Project description:Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer

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Determine the methyltransferase activities of METTL16 via MeRIP-seq (m6A-seq)

Project description:METTL16 belongs to methyltransferase like (METTL) family and could install m6A marks on its substrates. Here, we uncover a tumor-promoting role of METTL16 in AML and LSC self-renewal. To explore the mechanism underlying the oncogenic function of METTL16 in AML, we performed m6A-seq and RNA-seq. Via integrated analysis of m6A-seq data and RNA-seq data, we identified two bona fide targets of METTL16, BCAT1 and BCAT2. METTL16 functions as an m6A methyltransferase to regulate expression of BCAT1 and BCAT2, which contribute to reprogramming of BCAA metabolism.

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Determine METTL16-mediated spatiotemoral installation of m6A via MeRIP-seq (m6A-seq) with nascent RNA and nuclear poly(A) RNA

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Mettl16 promotes hematopoietic stem and progenitor cell expansion in embryonic hematopoiesis [m6A-Seq]

Project description:The RNA N6-methyladenosine (m6A) modification has emerged as an essential regulator of vertebrate embryogenesis and malignancies. However, its functions and underlying molecular mechanisms in the expansion of hematopoietic stem and progenitor cells (HSPCs) during early embryonic development remain elusive. Here we show that Mettl16, an RNA methyltransferase identified recently, is specifically required for HSPC expansion during zebrafish early embryonic development in an m6A-dependent manner. In mettl16 deficient embryos, HSPCs exhibit defective proliferation capacity due to G0/G1 arrest. Mechanistically, HSPC proliferation is blocked by impaired methyltransferase function of Mettl16 in vivo. We identify cell cycle gene mybl2b as a novel direct m6A target of Mettl16, and Mettl16 deficiency destabilizes mybl2b mRNA, which is mediated by m6A reader Igf2bp1. Moreover, we revealed that the METTL16-m6A-MYBL2-IGF2BP1 signaling axis in G1/S progression is conserved in humans. Collectively, our findings demonstrate the critical function of m6A modification deposited by Mettl16 in HSPC expansion during early embryonic development.

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METTL16 is a N6-methyladenosine (m6A) methyltransferase that targets pre-mRNAs and various non-coding RNAs

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Project description:Internal modification of RNAs with N6-methyladenosine (m6A) is a highly conserved and widely used means of gene expression control. METTL16 is an m6A writer but how it recognizes its RNA targets and its physiological roles remain unknown. Here we describe the crystal structure of human METTL16 to reveal a classical methyltransferase domain but with an extra N-terminal module that is essential for catalysis. Together, they form a deep-cut groove lined by highly conserved positively charged residues that are essential for RNA binding and methylation activity. When given a random pool of RNAs, METTL16 selects structured RNAs for m6A methylation. We demonstrate that mouse Mettl16 is essential for early embryonic development, and acts via regulation of the SAM synthetase Mat2a mRNA. Our results highlight the pivotal role of an m6A RNA methyltransferase in facilitating early developmental decisions via regulation of SAM availability.

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