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- W3100284702 abstract "Eukaryotic transfer RNAs can become selectively fragmented upon various stresses, generating tRNA-derived small RNA fragments. Such fragmentation has been reported to impact a small fraction of the tRNA pool and thus presumed to not directly impact translation. We report that oxidative stress can rapidly generate tyrosine-tRNAGUA fragments in human cells-causing significant depletion of the precursor tRNA. Tyrosine-tRNAGUA depletion impaired translation of growth and metabolic genes enriched in cognate tyrosine codons. Depletion of tyrosine tRNAGUA or its translationally regulated targets USP3 and SCD repressed proliferation-revealing a dedicated tRNA-regulated growth-suppressive pathway for oxidative stress response. Tyrosine fragments are generated in a DIS3L2 exoribonuclease-dependent manner and inhibit hnRNPA1-mediated transcript destabilization. Moreover, tyrosine fragmentation is conserved in C. elegans. Thus, tRNA fragmentation can coordinately generate trans-acting small RNAs and functionally deplete a tRNA. Our findings reveal the existence of an underlying adaptive codon-based regulatory response inherent to the genetic code." @default.
- W3100284702 created "2020-11-23" @default.
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- W3100284702 date "2020-12-21" @default.
- W3100284702 modified "2023-10-11" @default.
- W3100284702 title "A stress‐induced tyrosine‐tRNA depletion response mediates codon‐based translational repression and growth suppression" @default.
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- W3100284702 doi "https://doi.org/10.15252/embj.2020106696" @default.
- W3100284702 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7809793" @default.
- W3100284702 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33346941" @default.
- W3100284702 hasPublicationYear "2020" @default.