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MDA5 guards against infection by surveying cellular RNA homeostasis [I]

ABSTRACT: MDA5 guards against infection by surveying cellular RNA homeostasis [I]

PROVIDER: PRJNA869666 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21052255_1.fastq.gz	Fastqsanger.gz
	SRR21052255_2.fastq.gz	Fastqsanger.gz
	SRR21052256_1.fastq.gz	Fastqsanger.gz
	SRR21052256_2.fastq.gz	Fastqsanger.gz
	SRR21052257_1.fastq.gz	Fastqsanger.gz

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MDA5 guards against infection by surveying cellular RNA homeostasis

Project description:MDA5 guards against infection by surveying cellular RNA homeostasis

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MDA5 guards against infection by surveying cellular RNA homeostasis [II]

Project description:MDA5 guards against infection by surveying cellular RNA homeostasis [II]

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MDA5 guards against infection by surveying cellular RNA homeostasis [II]

Project description:MDA5 is an innate immune RNA sensor that detects a range of viruses. MDA5’s RNA agonists are not well defined. We used individual-nucleotide resolution crosslinking and immunoprecipitation (iCLIP) to study its ligands. Surprisingly, upon infection with SARS-CoV-2 or encephalomyocarditis virus (EMCV), MDA5 bound overwhelmingly to cellular RNAs. Many binding sites were intronic and proximal to Alu elements. MDA5-bound RNA was enriched in Poly(A) and Poly(U) motifs, some of which may form double-stranded RNA. In EMCV-infected cells, cytoplasmic levels of intron-containing unspliced transcripts were increased, suggesting dysregulation of splicing. Concomitantly, MDA5 iCLIP peaks were enriched in introns accumulating in the cytoplasm of infected cells. Moreover, rescue of splicing abrogated MDA5 activation. Finally, depletion of viral RNA from RNA extracted from infected cells did not diminish its MDA5-stimulatory potential. Taken together, MDA5 surveys RNA processing fidelity and detects splicing perturbation during infection, establishing a paradigm of innate immune ‘guarding’ for RNA sensors.

2023-11-29 | GSE214663 | GEO

MDA5 guards against infection by surveying cellular RNA homeostasis [I]

2023-11-29 | GSE211240 | GEO

MDA5 guards against infection by surveying cellular RNA homeostasis

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2023-11-28 | GSE214664 | GEO

Transcription profiling of brains from honey bees guards of different subspecies and host colony environment

Project description:Expression profiling of guards brains as a function of individual genotype (AHB/EHB) and environment (AHB/EHB host colony)

2009-07-01 | E-TABM-606 | biostudies-arrayexpress

Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [ADAR1KO HEK293T and WT MDA5]

Project description:Aberrant activation of innate immune receptors can cause a spectrum of immune disorders, such as Aicardi-Goutières syndrome (AGS). One such receptor is MDA5, a viral double-stranded RNA (dsRNA) sensor that induces antiviral immune response. We here demonstrate that constitutive activation of MDA5 in AGS results from the loss of tolerance to cellular dsRNAs formed by Alu retroelements. While wild-type MDA5 cannot efficiently recognize Alu-dsRNA because its filament formation on dsRNA is impaired by the imperfect duplex structure, AGS-variants of MDA5 display reduced sensitivity to duplex structural irregularities, assembling signaling-competent filaments on Alu-dsRNA. Moreover, we identified an unexpected role of RNA-rich cellular environment in suppressing aberrant MDA5 oligomerization, highlighting context-dependence of self vs. non-self discrimination. Overall, our work demonstrates that the increased efficiency of MDA5 to recognize dsRNA comes at a cost of self-recognition, and implicates a unique role of Alu RNAs as virus-like elements that shape the primate immune system.

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Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [WT HEK293T and mutant MDA5]

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Surveying WOR-3 Bacteria

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Project description:Tendons are vital collagen-dense specialized connective tissues transducing the force from skeletal muscle to the bone, thus enabling movement of the human body. Tendon cells adjust matrix turnover in response to physiological tissue loading and pathological overloading (tendinopathy). Nevertheless, the regulation of tendon matrix quality control is still poorly understood and the pathogenesis of tendinopathy is presently unsolved. Autophagy, the major mechanism of degradation and recycling of cellular components, plays a fundamental role in the homeostasis of several tissues. Here, we investigate the contribution of autophagy to human tendons' physiology, and we provide in vivo evidence that it is an active process in human tendon tissue. We show that selective autophagy of the endoplasmic reticulum (ER-phagy), regulates the secretion of type I procollagen (PC1), the major component of tendon extracellular matrix. Pharmacological activation of autophagy by inhibition of mTOR pathway alters the ultrastructural morphology of three-dimensional tissue-engineered tendons, shifting collagen fibrils size distribution. Moreover, autophagy induction negatively affects the biomechanical properties of the tissue-engineered tendons, causing a reduction in mechanical strength under tensile force. Overall, our results provide the first evidence that autophagy regulates tendon homeostasis by controlling PC1 quality control, thus potentially playing a role in the development of injured tendons.

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