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PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [Polysome profiling]

ABSTRACT: PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [Polysome profiling]

PROVIDER: PRJNA1231450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR32566339_1.fastq.gz	Fastqsanger.gz
	SRR32566339_2.fastq.gz	Fastqsanger.gz
	SRR32566340_1.fastq.gz	Fastqsanger.gz
	SRR32566340_2.fastq.gz	Fastqsanger.gz

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PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [Polysome profiling]

Project description:Pseudouridine (Y) is the most widespread RNA modification type on cellular RNAs and is dynamically catalyzed by a family of Y synthases (PUSes) in response to pathophysiological cues. PUS10 has been previously shown to regulate miRNA biogenesis in addition to modifying tRNAs, however its role in adapting gene expression to stress remains elusive. Here, we establish a novel role for PUS10 as a regulator of LTR retrotransposon-driven inflammatory response. Using Pus10 KO mice, we demonstrate that Pus10 depletion leads to upregulation of interferon-stimulated genes (ISGs) and increased resistance to viral infection in vitro and in vivo. Mechanistically, PUS10 regulates a subset of 5’-derived tRNA (tdR) fragment, 5’ tdR Gly-GCC, that via targeting specific LTR retroelements modulates RNA-DNA hybrids accumulation and cGAS/STING/IRF3 pathway. Importantly, reduced PUS10 activity correlate with chronic autoimmune conditions, pinpointing PUS10 as a potential contributor to human immune regulation.

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PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation

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Project description:Pseudouridine synthases (PUSs) catalyze the isomerization of uridine (U)-to-pseudouridine (Ψ) and have emerging roles in development and disease. How PUSs adapt gene expression under stress remains mostly unexplored. We identify an unconventional role for the Ψ “writer” PUS10 impacting intracellular innate immunity. Using Pus10 knock-out mice, we uncover cell-intrinsic upregulation of interferon (IFN) signalling, conferring resistance to inflammation in vivo. Pus10 loss alters tRNA-derived small RNAs (tdRs) abundance, perturbing translation and endogenous retroelements expression. We found one of the differentially expressed tDRs is derived from tRNA glycine (tDR Gly). To delinate the tDR Gly interactome, we employed an optimized pull-down strategy using PUS10 KO cells followed by data-independent acquisition-based quantitative mass spectrometry analysis.

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