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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

ABSTRACT: Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

PROVIDER: PRJNA1044762 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26941047_1.fastq.gz	Fastqsanger.gz
	SRR26941047_2.fastq.gz	Fastqsanger.gz
	SRR26941048_1.fastq.gz	Fastqsanger.gz
	SRR26941048_2.fastq.gz	Fastqsanger.gz
	SRR26941049_1.fastq.gz	Fastqsanger.gz

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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

Project description:Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

Project description:The role of Argonaute (AGO) proteins and the RNA interference (RNAi) machinery in mammalian antiviral response has been debated. Therefore, we set out to investigate how mammalian RNAi impacts influenza A virus (IAV) infection. We demonstrate that IAV infection triggers nuclear accumulation of AGO2, which is directly facilitated by p53 activation. Mechanistically, we show that IAV induces nuclear AGO2 targeting of TRIM71, a proposed AGO2 E3 ligase, and type-I interferon-pathway genes for silencing. Hence, the RNAi machinery is highjacked by the virus to evade the immune system and support viral replication. We demonstrate that the FDA approved drug arsenic trioxide prevents nuclear AGO2:p53 accumulation, thereby increasing interferon response and decreasing viral replication in vitro and in a mouse model in vivo. Our data indicates that targeting the AGO2:p53-mediated silencing of innate immunity may offer a promising strategy to mitigate viral infections.

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Nuclear AGO2 Supports Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

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Nuclear RNAi Modulates Influenza A Virus Infectivity By Downregulating Type-I Interferon Response

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Influenza virus facilitates its infectivity by activating p53 to inhibit the expression of interferon-induced transmembrane proteins (IFITMs)

Project description:Transcriptome analysis of mock or H1N1 IAV PR8 infected p53WT A549 and p53null A549-KO3 cells by Affymetrix GeneChip Human Transcriptome 2.0 Arrays to achieve a set of genes those are regulated by p53 and responsive to IAV infection. Influenza A virus infection activates cellular p53, however it has not been clear whether this process has pro- or anti- viral effects. In this study, using human isogenic p53 wildtype A549 cells and p53null A549-KO3 cells generated from the CRISPR/Cas9 technology, we report that p53null cells exhibit significantly reduced viral propagation property when infected with influenza A virus (H1N1/A/Puerto Rico/8/34). Here, using genome-wide microarray analysis we revealed that p53 regulates the expression of a large set of interferon-inducible genes, some of which are directly associated with viral infectivity and later experimentally validated to be responsible for p53-regulated IAV infectivity.

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Project description:The reduced sperm count observed in Ago2 cKO mice implies that AGO2 has non-redundant functions in the male germ line. Because AGO2 is a key protein in the RNA interference (RNAi) pathway, we first postulated that AGO2 loss disrupts normal transcriptional and translational dynamics of target mRNAs relevant to sperm maturation. To address this hypothesis, we took advantage of the apparently normal spermatogenesis in Ago2 cKO mice, which allowed us to purify matched meiotic and post-meiotic germ cells from Ago2 cKO and wild type controls. We examined changes in the transcriptome and proteome of these two spermatogenic stages in Ago2 cKO relative to control mice using RNA-seq and quantitative mass spectrometry (MS). To further examine if the changes in mRNA and protein levels detected in Ago2 cKO germ cells was due to a loss of regulation by the canonical AGO2-miRNA pathway, we characterized AGO2 protein interactors by AGO2 immunoprecipitation-mass spectrometry (IP-MS) in cytoplasmic and nuclear fractions of post-meiotic cells

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