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Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections I

ABSTRACT: Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections I

PROVIDER: PRJNA804132 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17913813.fastq.gz	Fastqsanger.gz
	SRR17913814.fastq.gz	Fastqsanger.gz
	SRR17913815.fastq.gz	Fastqsanger.gz
	SRR17913816.fastq.gz	Fastqsanger.gz
	SRR17913817.fastq.gz	Fastqsanger.gz

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Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections I

Project description:N6-methyladenosine (m6A) is a dynamic post-transcriptional RNA modification influencing all aspects of mRNA biology. Here, we examined cellular m6A epitranscriptomes during infections of herpes simplex virus type 1 (HSV-1) and lipopolysaccharide (LPS) stimulation to identify m6A-regulated innate immune response genes. We showed that a significant portion of cellular genes including many innate immune response genes underwent m6A modifications in 5’UTR and 3’UTR, from which we identified common and distinct m6A-modified genes under different stimulating conditions.

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Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial Infections II

Project description:N6-methyladenosine (m6A) is a dynamic post-transcriptional RNA modification influencing all aspects of mRNA biology. Here, we examined cellular m6A epitranscriptomes during P.aeruginosa infection to identify m6A-regulated innate immune response genes with or without ALKBH5 knockdown. We showed that a significant portion of cellular genes including many innate immune response genes underwent m6A modifications in 5’UTR and 3’UTR, from which we identified common and distinct m6A-modified genes under different stimulating conditions.

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Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial Infections II

Project description:Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial Infections II

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Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections

Project description:Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections

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N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

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Project description:N6-methyladenosine (m6A), the most abundant messenger RNA (mRNA) modification, has emerged as a critical post-transcriptional mechanism that regulates various aspect of mRNA metabolism including pre-mRNA processing, mRNA export, mRNA stability and translation efficiency. However the genetics basis of m6A is largely unexplored. In this work, we mapped m6A-QTLs in 60 LCLs and used the resulting tens of thousands of QTLs to provide insights to m6A biology and its contribution to human complex trait.

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