MassIVE MSV000095557

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Transfer RNA acetylation regulates in vivo mammalian stress signaling

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Description

Transfer RNA (tRNA) modifications are crucial for protein synthesis, but their physiological roles remain poorly understood. Here we investigate the impact of N4-acetylcytidine (ac4C), a highly conserved tRNA modification, using a Thumpd1 knockout mouse model. We find that loss of Thumpd1-dependent tRNA acetylation leads to reduced levels of tRNALeu, increased ribosome stalling, and activation of eIF2-alpha phosphorylation. Thumpd1 knockout mice exhibit growth defects and sterility. Remarkably, concurrent knockout of Thumpd1 and the stress-sensing kinase Gcn2 causes penetrant postnatal lethality, revealing a critical genetic interaction. Our findings demonstrate that a modification restricted to a single position within type II cytosolic tRNAs can regulate ribosome-mediated signaling in mammalian organisms. Insights into how tRNA modifications shape phenotype and signaling in response to stress provide a foundation for novel strategies for therapeutic intervention and translational control. [doi:10.25345/C5CC0V528] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Thumpd1, tRNA, N4-acetylcytidine

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Principal Investigators:
(in alphabetical order) 		Jordan Meier, National Cancer Institute, USA
Submitting User: ronholes7059
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