The Greatwall-Endosulfine-PP2A/B55 pathway regulates entry into quiescence by enhancing translation of Elongator-tunable transcripts

Javier Encinar del Dedo (), M. Belén Suárez, Rafael López-San Segundo, Alicia Vázquez-Bolado, Jingjing Sun, Natalia García-Blanco, Patricia García, Pauline Tricquet, Jun-Song Chen, Peter C. Dedon, Kathleen L. Gould, Elena Hidalgo, Damien Hermand and Sergio Moreno ()
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Javier Encinar del Dedo: University of Salamanca
M. Belén Suárez: CSIC
Rafael López-San Segundo: University of Salamanca
Alicia Vázquez-Bolado: University of Salamanca
Jingjing Sun: Singapore-MIT Alliance for Research and Technology
Natalia García-Blanco: University of Salamanca
Patricia García: CSIC
Pauline Tricquet: University of Namur
Jun-Song Chen: Vanderbilt University School of Medicine
Peter C. Dedon: Singapore-MIT Alliance for Research and Technology
Kathleen L. Gould: Vanderbilt University School of Medicine
Elena Hidalgo: Universitat Pompeu Fabra
Damien Hermand: University of Namur
Sergio Moreno: University of Salamanca

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract Quiescent cells require a continuous supply of proteins to maintain protein homeostasis. In fission yeast, entry into quiescence is triggered by nitrogen stress, leading to the inactivation of TORC1 and the activation of TORC2. In this study, we demonstrate that the Greatwall-Endosulfine-PPA/B55 pathway connects the downregulation of TORC1 with the upregulation of TORC2, resulting in the activation of Elongator-dependent tRNA modifications crucial for sustaining the translation programme during entry into quiescence. This mechanism promotes U34 and A37 tRNA modifications at the anticodon stem loop, enhancing translation efficiency and fidelity of mRNAs enriched for AAA versus AAG lysine codons. Notably, several of these mRNAs encode TORC1 inhibitors, TORC2 activators, tRNA modifiers, and proteins necessary for telomeric and subtelomeric functions. Therefore, we propose a mechanism by which cells respond to nitrogen stress at the level of translation, involving a coordinated interplay between tRNA epitranscriptome and biased codon usage.

Date: 2024
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DOI: 10.1038/s41467-024-55004-4

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