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PUS10 driven tRNA fragmentation mediates transposon induced inflamation [HSC RNA-seq]

ABSTRACT: PUS10 driven tRNA fragmentation mediates transposon induced inflamation [HSC RNA-seq]

PROVIDER: PRJNA1132982 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29735830_1.fastq.gz	Fastqsanger.gz
	SRR29735830_2.fastq.gz	Fastqsanger.gz
	SRR29735831_1.fastq.gz	Fastqsanger.gz
	SRR29735831_2.fastq.gz	Fastqsanger.gz
	SRR29735832_1.fastq.gz	Fastqsanger.gz

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PUS10 driven tRNA fragmentation mediates transposon induced inflamation [HSC RNA-seq]

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 [RNA-seq]

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 knockout mice, we uncover cell-intrinsic upregulation of interferon (IFN) signaling, conferring resistance to inflammation in vivo. Pus10 loss alters tRNA-derived small RNAs (tdRs) abundance, perturbing translation and endogenous retroelements expression. These alterations promote proinflammatory RNA-DNA hybrids accumulation, potentially activating cyclic GMP-AMP synthase (cGAS)-stimulator of interferon gene (STING). Supplementation with selected tdR pools partly rescues these effects through interactions with RNA processing factors that modulate immune responses, revealing a regulatory circuit that counteracts cell-intrinsic inflammation. By extension, we define a PUS10-specific molecular fingerprint linking its dysregulation to human autoimmune disorders, including inflammatory bowel diseases. Collectively, these findings establish PUS10 as a viral mimicry modulator, with broad implications for innate immune homeostasis and autoimmunity.

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