Reciprocal regulation of TORC signaling and tRNA modifications by Elongator enforces nutrient-dependent cell fate.
Cell Differentiation
/ genetics
Cell Proliferation
/ genetics
Gene Expression Regulation, Fungal
/ genetics
Glycogen Synthase Kinase 3
/ genetics
Mechanistic Target of Rapamycin Complex 1
/ genetics
Mechanistic Target of Rapamycin Complex 2
/ genetics
Mitosis
/ genetics
Nutrients
/ genetics
Peptide Chain Elongation, Translational
/ genetics
Phosphorylation
/ genetics
RNA, Transfer
/ genetics
Schizosaccharomyces
/ genetics
Signal Transduction
/ genetics
Journal
Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
06
08
2018
accepted:
14
05
2019
entrez:
22
6
2019
pubmed:
22
6
2019
medline:
30
4
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 31223645
doi: 10.1126/sciadv.aav0184
pii: aav0184
pmc: PMC6584457
doi:
Substances chimiques
RNA, Transfer
9014-25-9
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Mechanistic Target of Rapamycin Complex 2
EC 2.7.11.1
Glycogen Synthase Kinase 3
EC 2.7.11.26
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
eaav0184Subventions
Organisme : NIEHS NIH HHS
ID : R01 ES026856
Pays : United States
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