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FTO-mediated RNA m6A demethylation regulates aggressive behavior and inflammation of fibroblast-like synoviocytes

ABSTRACT: FTO-mediated RNA m6A demethylation regulates aggressive behavior and inflammation of fibroblast-like synoviocytes

PROVIDER: PRJNA1007578 | ENA |

REPOSITORIES: ENA

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Transcriptome profile of fibroblast-like synoviocytes with FTO knockdown

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m6A modification profiles in RA FLS with FTO knockdown

Project description:Fibroblast-like synoviocytes (FLS) harbour active migration, invasion, proliferation and decreased cell-contact inhibition, and served as a crucial component in pathogenesis of rheumatoid arthritis. However, the mechanism underlying the aggressive behavior remain unclear. In this study, we established FTO-knockdown RA FLS to investigate the molecular mechanism.

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FTO-mediated RNA m6A demethylation regulates aggressive behavior and inflammation of fibroblast-like synoviocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

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FTO mediates LINE1 m6A demethylation and chromatin regulation in mESCs and mouse development

Project description:N6-methyladenosine (m6A) is the most abundant internal modification on mammalian messenger RNA (mRNA). It is installed by a writer complex and can be reversed by erasers such as the fat mass and obesity-associated protein (FTO). Despite extensive research, the primary physiological substrates of FTO in mammalian tissues and development remain elusive. Here, we show that FTO mediates m6A demethylation of long-interspersed element-1 (LINE1) RNA in mouse embryonic stem cells (mESCs), regulating LINE1 RNA abundance and the local chromatin state, which in turn modulates transcription of LINE1-containing genes. FTO-mediated LINE1 RNA m6A demethylation also plays regulatory roles in shaping chromatin state and gene expression during mouse oocyte and embryonic development. Our results suggest broad effects of LINE1 RNA m6A demethylation by FTO in mammals.

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Differential m6A, m6Am, and m1A Demethylation Mediated by FTO in Cell Nucleus and Cytoplasm

Project description:FTO, the first RNA demethylase discovered, mediates the demethylation of N6-methyladenosine (m6A), installed internally on messenger RNA, and N6,2′-O-dimethyladenosine (m6Am), occurring at the +1 position from the 5’ cap. Despite extensive recent research on FTO, its physiological impact on cellular processes has yet to be fully elucidated. Here, we demonstrate that the cellular distribution of FTO is distinct among different cell lines, which critically affects the access of FTO to different RNA substrates. FTO binds multiple RNA substrates, including mRNA, U6 RNA, and tRNA. It mainly targets internal m6A when located in the cell nucleus and preferentially demethylates m6Am when residing in the cytoplasm. The expression levels of transcripts containing internal m6A are associated with the alteration of the FTO more so than transcripts containing m6Am. We also discover that N1-methyladenosine (m1A) in tRNA is a main substrate of FTO, with the FTO-catalyzed demethylation of target tRNAs repressing protein synthesis. Collectively, FTO-mediated RNA demethylation affects both mRNA level and translation through distinct pathways.

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SFPQ is a FTO binding protein that assists specific m6A demethylation

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Quantitative Proteomics of Mouse Liver (FTO-KO,WT) in response to DEN injection

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FTO mediates LINE1 m6A demethylation and chromatin regulation in mESCs and mouse tissues

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Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from FTO knockout mice

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