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Sci Adv. 2019 Jun 19;5(6):eaav0184. doi: 10.1126/sciadv.aav0184. eCollection 2019 Jun.

Reciprocal regulation of TORC signaling and tRNA modifications by Elongator enforces nutrient-dependent cell fate.

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URPHYM-GEMO, University of Namur, rue de Bruxelles, 61, Namur 5000, Belgium.
Singapore-MIT Alliance for Research and Technology Centre (SMART), Center for Life Sciences 05-06, 28 Medical Drive, 117456 Singapore.
Massachusetts Institute of Technology, 56-787B77 Massachusetts Avenue, Cambridge, MA 02139-4307, USA.
Division of Biological Science, Nara Institute of Science and Technology, Ikoma, Nara 630-0192, Japan.
Department of Microbiology and Molecular Genetics, University of California, Davis, CA 95616, USA.


Nutrient availability has a profound impact on cell fate. Upon nitrogen starvation, wild-type fission yeast cells uncouple cell growth from cell division to generate small, round-shaped cells that are competent for sexual differentiation. The TORC1 (TOR complex 1) and TORC2 complexes exert opposite controls on cell growth and cell differentiation, but little is known about how their activity is coordinated. We show that transfer RNA (tRNA) modifications by Elongator are critical for this regulation by promoting the translation of both key components of TORC2 and repressors of TORC1. We further identified the TORC2 pathway as an activator of Elongator by down-regulating a Gsk3 (glycogen synthase kinase 3)-dependent inhibitory phosphorylation of Elongator. Therefore, a feedback control is operating between TOR complex (TORC) signaling and tRNA modification by Elongator to enforce the advancement of mitosis that precedes cell differentiation.

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