A tRNA half modulates translation as stress response in Trypanosoma brucei

In the absence of extensive transcription control mechanisms the pathogenic parasite Trypanosoma brucei crucially depends on translation regulation to orchestrate gene expression. However, molecular insight into regulating protein biosynthesis is sparse. Here we analyze the small non-coding RNA (ncR...

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Veröffentlicht in:Nature communications 2019-01, Vol.10 (1), p.118-118, Article 118
Hauptverfasser: Fricker, Roger, Brogli, Rebecca, Luidalepp, Hannes, Wyss, Leander, Fasnacht, Michel, Joss, Oliver, Zywicki, Marek, Helm, Mark, Schneider, André, Cristodero, Marina, Polacek, Norbert
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Sprache:eng
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Zusammenfassung:In the absence of extensive transcription control mechanisms the pathogenic parasite Trypanosoma brucei crucially depends on translation regulation to orchestrate gene expression. However, molecular insight into regulating protein biosynthesis is sparse. Here we analyze the small non-coding RNA (ncRNA) interactome of ribosomes in T. brucei during different growth conditions and life stages. Ribosome-associated ncRNAs have recently been recognized as unprecedented regulators of ribosome functions. Our data show that the tRNA Thr 3´half is produced during nutrient deprivation and becomes one of the most abundant tRNA-derived RNA fragments (tdRs). tRNA Thr halves associate with ribosomes and polysomes and stimulate translation by facilitating mRNA loading during stress recovery once starvation conditions ceased. Blocking or depleting the endogenous tRNA Thr halves mitigates this stimulatory effect both in vivo and in vitro . T. brucei and its close relatives lack the well-described mammalian enzymes for tRNA half processing, thus hinting at a unique tdR biogenesis in these parasites. Trypanosoma brucei mainly relies on translational regulation to adjust gene expression, but details are unclear. Here the authors show that, under stress conditions, tRNA Thr half level increases, associates with ribosomes and polysomes, and stimulates protein synthesis by facilitating mRNA loading.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-018-07949-6