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Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2 [scRNA-Seq]

ABSTRACT: Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2 [scRNA-Seq]

PROVIDER: PRJNA922193 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23029630_1.fastq.gz	Fastqsanger.gz
	SRR23029630_2.fastq.gz	Fastqsanger.gz
	SRR23029631_1.fastq.gz	Fastqsanger.gz
	SRR23029631_2.fastq.gz	Fastqsanger.gz
	SRR23029632_1.fastq.gz	Fastqsanger.gz

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Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2

Project description:Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2

| PRJNA922192 | ENA

Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2 [RNA-Seq]

Project description:Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2 [RNA-Seq]

| PRJNA919019 | ENA

Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2 [scRNA-Seq]

Project description:Under normal homeostatic conditions, self double-stranded RNA (self-dsRNA) is modified by adenosine deaminase acting on RNA 1 (ADAR1) to prevent the induction of a type I interferon (IFN) mediated inflammatory cascade. Antigen presenting cells (APCs) sense pathogen associated molecular patterns (PAMPs), such as dsRNA, to activate the immune response. The impact of ADAR1 on the function of APCs and the consequences on immunity is poorly understood. Here, we show that ADAR1 deletion in CD11c+ APCs leads to: (i) a skewed myeloid cell compartment enriched in inflammatory cDC2s (inf-cDC2) like cells; (ii) enhanced numbers of activated tissue resident memory T cells (TRMs) in the lung; and (iii) the imprinting of a broad antiviral transcriptional signature across both immune and non-immune cells. Further the resulting changes can be partially reversed by blocking IFNAR1 signaling and promote early resistance against SARS-CoV-2 infection. Our study provides insight into the consequences of self-dsRNA sensing in APCs on the immune system in the context of viral challenge.

2023-01-22 | GSE222487 | GEO

Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2 [RNA-Seq]

2023-01-22 | GSE222326 | GEO

Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2.

Project description: Not available

| S-EPMC9842623 | biostudies-literature

ADAR1 biology can hinder effective antiviral RNA interference

Project description:Viruses constantly evolve and adapt to the antiviral defenses of their hosts. The biology of viral circumvention of these selective pressures can often be attributed to the acquisition of novel antagonistic gene products or by rapid genome change that prevents host recognition. To study viral evasion of RNA interference (RNAi)-based defenses, we established a robust antiviral system in mammalian cells using recombinant Sendai virus designed to be targeted by endogenous host microRNAs (miRNAs) with perfect complementarity. Using this system, we previously demonstrated the intrinsic ability of positive-strand RNA viruses to escape this selective pressure via homologous recombination, which was not observed in negative-strand RNA viruses. Here we show that given extensive time, escape of miRNA-targeted Sendai virus was enabled by host adenosine deaminase acting on RNA 1 (ADAR1). Independent of the viral transcript targeted, ADAR1 editing resulted in disruption of the miRNA-silencing motif, suggesting an intolerance for extensive RNA:RNA interactions necessary for antiviral RNAi. This was further supported in N. benthamiana, where exogenous expression of ADAR1 interfered with endogenous RNAi. Together, these results suggest that ADAR1 diminishes the effectiveness of RNAi and may explain why it is absent in species that utilize this antiviral defense system.

2023-03-21 | GSE227592 | GEO

ADAR1 biology can hinder effective antiviral RNA interference

Project description:ADAR1 biology can hinder effective antiviral RNA interference

| PRJNA945880 | ENA

Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2

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

2023-01-22 | GSE222489 | GEO

Irf7 orchestrates the immunological reaction in cardiomyocytes upon Adar1 deletion

Project description:Adenosine deaminases acting on RNA (Adar1 and Adar2) catalyze I-to-A RNA editing, a post-transcriptional mechanism involved in multiple cellular functions. The role of Adar1-dependent RNA editing in cardiomyocytes (CMs) remains unclear. Here we show that conditional deletion of Adar1 in CMs results in myocarditis progressively evolving into dilated cardiomyopathy and heart failure at only 6 months of age. Adar1 depletion drives activation of interferon signaling genes (ISGs) in the absence of apoptosis and cytokine activation, and reduces the hypertrophic response of CMs upon pressure overload. Interestingly, ablation of the cytosolic sensor MDA5 prevents cardiac ISG activation and delays disease onset, but does not rescue the long-term lethal phenotype elicited by conditional deletion of Adar1. Retention of a single catalytically inactive Adar1 allele in CMs, in combination with MDA5 depletion, however, completely restores the cardiac function and prevents heart failure. Finally, ablation of interferon regulatory factor 7 (Irf7) attenuates the phenotype of Adar1-deficient CMs to a similar extent as MDA5 depletion, highlighting Irf7 as the main regulator of the immune response triggered by lack of Adar1 in CMs.

2022-08-24 | PXD024974 | Pride

The RNA editing enzyme ADAR1 is a key regulatory of innate immune responses to RNA

Project description:The ADAR RNA editing enzymes deaminate adenosine bases to inosines in cellular RNAs, recoding open reading frames. Human ADAR1 mutations cause Aicardi-Goutieres Syndrome (AGS) and Adar1 mutant mice showing an aberrant interferon response and death by embryonic day E12.5 model the human disease. Searches have not identified key ADAR1 RNA editing sites recoding immune/haematopoietic proteins but editing is widespread in Alu sequences. We show that Adar1 embryonic lethality is rescued in Adar1; Mavs double mutant mice in which general antiviral responses to cytoplasmic dsRNA are prevented. We propose that inosine bases are epigenetic marks identifying cellular RNA as innate immune ÒselfÓ. Consistent with this idea we show that an editing-active cytoplasmic ADAR is required to prevent aberrant immune responses in Adar1 mutant mouse embryo fibroblasts. No dramatic increase in repetitive transcripts is observed. AGS mutations in ADAR1 affect editing by the interferon-inducible cytoplasmic ADAR1 isoform. RNA-seq expression profiling in Adar1 and Adar1/Mavs knockout mice embryos.

2014-12-19 | E-GEOD-62917 | biostudies-arrayexpress

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