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Gut microbiota rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

ABSTRACT: Gut microbiota rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

PROVIDER: PRJNA901900 | ENA |

REPOSITORIES: ENA

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Gut microbiota rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host's mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.

2024-04-21 | GSE218001 | GEO

Gut microbiota dysbiosis rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

Project description:Gut microbiota dysbiosis rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

| PRJNA894523 | ENA

Gut microbiota dysbiosis rewires host mRNA m6A epitranscriptomic landscape via bile acid metabolism

Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host′s mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.

2024-04-21 | GSE216620 | GEO

Impact of gut microbiota on m6A/m epitranscriptomic mRNA modification in different host tissues

Project description:In this study we performed MeRIP-Seq to study N6-methyl adenosine (m6A) and and N6,2′ -O-dimethyladenosine (m6Am) modification of mRNA. We investigated the effect of the microbiota on the transcriptome and epitranscriptomic modifications in murine liver and cecum. We compared m6A/m modification profiles in cecum of conventionally raised (CONV) and germ-free (GF) mice. We additionally included GF mice colonised with the flora of CONV mice for four weeks (ex-GF), for which show that they exhibit similar patterns of the most abundant genera of gut bacteria as CONV mice. We added mice treated with several antibiotics to deplete the gut flora (abx)and vancomycin treated mice in which the genera Akkermansia, Escherichia/Shigella and Lactobacillus were enriched. Furthermore, we included GF mice colonised with the commensal bacterium Akkermansia muciniphila (Am), Lactobacillus plantarum (Lp) and Escherichia coli Nissle (Ec) and analysed their m6A/m modification profiles. In addition, we analysed changes in m6A/m- modified liver RNA for CONV, GF, and Am, Lp and Ec mice.

2020-02-12 | E-MTAB-6560 | biostudies-arrayexpress

m6A-mRNA&lncRNA Epitranscriptomic Microarray

Project description:m6A-mRNA&lncRNA Epitranscriptomic Microarray

| PRJNA774778 | ENA

m6A-mRNA&lncRNA Epitranscriptomic Microarray

Project description:Total RNA samples from human bronchial epithelial BEAS-2B passage-matched control cells and Cr(VI)-transofmred BEAS-2B cells were submitted to ArraySatr for total RNA m6A epitranscriptomic microarray analysis

2022-06-29 | GSE186605 | GEO

m6A Epitranscriptomic Microarray of primary mouse RPE cells treated with TGF-β2

Project description:m6A-mRNA&lncRNA Epitranscriptomic Microarray of primary mouse RPE cells comparing control untreated RPE cells with RPE cells treated with TGF-β2 at a concentration of 10 ng/ml. The goal was to determine the effects of RNA m6a methylation on primary mouse RPE cells undergoing epithelial-mesenchymal transition induced by TGF-β2.

2021-06-26 | GSE178946 | GEO

m6A-Epitranscriptomic Microarray analysis of CD11b+Mac-Spleen from HFD-Mettl3-LysM-Cre mice

Project description:We processed m6A-Epitranscriptomic Microarray analysis on splenic CD11b+ macrophages isolated from 10-week old Mettl3f/f-LysM-Cre KO and littermate WT mice.

2022-01-07 | GSE184367 | GEO

m6A epitranscriptomic mRNA modifications in host tissues and gut microbiota

Project description:Impact of gut microbiota on m6A epitranscriptomic mRNA modifications in host tissues

| PRJEB25135 | ENA

Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

Project description:Several prior reports have demonstrated that the epitranscriptomic addition of m6A to viral transcripts promotes the replication and pathogenicity of a wide range of viruses yet the underlying mechanism(s) causing this positive effect has remained unclear. It is known that m6A function is largely mediated by cellular m6A binding proteins or readers, however, how these m6A reader proteins contribute to the regulation of HIV-1 gene expression has remained controversial. Here, we confirm that m6A indeed enhances HIV-1 gene expression. We demonstrate that this effect is collectively mediated by the cytoplasmic reader YTHDF2, which increases HIV-1 transcript stability, and the nuclear m6A reader YTHDC1, which binds HIV-1 RNA at 7 distinct m6A methylated sites, regulating viral transcript alternative splicing.

2021-02-06 | GSE166237 | GEO

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