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

Identifieur interne : 000251 ( Main/Exploration ); précédent : 000250; suivant : 000252

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

Auteurs : Julie Candiracci [Belgique] ; Valerie Migeot [Belgique] ; Yok-Hian Chionh [Singapour] ; Fanelie Bauer [Belgique] ; Thomas Brochier [Belgique] ; Brandon Russell [États-Unis] ; Kazuhiro Shiozaki [Japon, États-Unis] ; Peter Dedon [Singapour, États-Unis] ; Damien Hermand [Belgique]

Source :

RBID : pubmed:31223645

Descripteurs français

English descriptors

Abstract

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.

DOI: 10.1126/sciadv.aav0184
PubMed: 31223645
PubMed Central: PMC6584457


Affiliations:


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Le document en format XML

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<term>Cell Proliferation (genetics)</term>
<term>Gene Expression Regulation, Fungal (genetics)</term>
<term>Glycogen Synthase Kinase 3 (genetics)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (genetics)</term>
<term>Mechanistic Target of Rapamycin Complex 2 (genetics)</term>
<term>Mitosis (genetics)</term>
<term>Nutrients (genetics)</term>
<term>Peptide Chain Elongation, Translational (genetics)</term>
<term>Phosphorylation (genetics)</term>
<term>RNA, Transfer (genetics)</term>
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<term>ARN de transfert (génétique)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (génétique)</term>
<term>Complexe-2 cible mécanistique de la rapamycine (génétique)</term>
<term>Différenciation cellulaire (génétique)</term>
<term>Glycogen Synthase Kinase 3 (génétique)</term>
<term>Mitose (génétique)</term>
<term>Nutriments (génétique)</term>
<term>Phosphorylation (génétique)</term>
<term>Prolifération cellulaire (génétique)</term>
<term>Régulation de l'expression des gènes fongiques (génétique)</term>
<term>Schizosaccharomyces (génétique)</term>
<term>Transduction du signal (génétique)</term>
<term>Élongation de la traduction (génétique)</term>
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<term>Cell Proliferation</term>
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<term>Nutrients</term>
<term>Peptide Chain Elongation, Translational</term>
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<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes fongiques</term>
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<div type="abstract" xml:lang="en">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.</div>
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