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

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

PROVIDER: PRJNA894523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22052500_1.fastq.gz	Fastqsanger.gz
	SRR22052500_2.fastq.gz	Fastqsanger.gz
	SRR22052501_1.fastq.gz	Fastqsanger.gz
	SRR22052501_2.fastq.gz	Fastqsanger.gz
	SRR22052502_1.fastq.gz	Fastqsanger.gz

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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.

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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.

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

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

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

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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.

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