RapamycinFungusV1, Main, Exploration, bibRecord, 000315

Integrated TORC1 and PKA signaling control the temporal activation of glucose-induced gene expression in yeast.

Identifieur interne : 000315 ( Main/Exploration ); précédent : 000314; suivant : 000316

Integrated TORC1 and PKA signaling control the temporal activation of glucose-induced gene expression in yeast.

Auteurs : Joseph Kunkel [États-Unis] ; Xiangxia Luo [États-Unis] ; Andrew P. Capaldi [États-Unis]

Source :

Nature communications [ 2041-1723 ] ; 2019.

RBID : pubmed:31395866

Descripteurs français

English descriptors

KwdEn :
- Cyclic AMP-Dependent Protein Kinases (metabolism), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (MeSH), Glucose (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Transcription Factors (metabolism).
MESH :
- chemical , metabolism : Cyclic AMP-Dependent Protein Kinases, Glucose, Saccharomyces cerevisiae Proteins, Transcription Factors.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Gene Expression Profiling, Gene Expression Regulation, Fungal, Signal Transduction.

Abstract

The growth rate of a yeast cell is controlled by the target of rapamycin kinase complex I (TORC1) and cAMP-dependent protein kinase (PKA) pathways. To determine how TORC1 and PKA cooperate to regulate cell growth, we performed temporal analysis of gene expression in yeast switched from a non-fermentable substrate, to glucose, in the presence and absence of TORC1 and PKA inhibitors. Quantitative analysis of these data reveals that PKA drives the expression of key cell growth genes during transitions into, and out of, the rapid growth state in glucose, while TORC1 is important for the steady-state expression of the same genes. This circuit design may enable yeast to set an exact growth rate based on the abundance of internal metabolites such as amino acids, via TORC1, but also adapt rapidly to changes in external nutrients, such as glucose, via PKA.

DOI: 10.1038/s41467-019-11540-y
PubMed: 31395866
PubMed Central: PMC6687784

Affiliations:

États-Unis

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Le document en format XML

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<term>Glucose (metabolism)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
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<front><div type="abstract" xml:lang="en">The growth rate of a yeast cell is controlled by the target of rapamycin kinase complex I (TORC1) and cAMP-dependent protein kinase (PKA) pathways. To determine how TORC1 and PKA cooperate to regulate cell growth, we performed temporal analysis of gene expression in yeast switched from a non-fermentable substrate, to glucose, in the presence and absence of TORC1 and PKA inhibitors. Quantitative analysis of these data reveals that PKA drives the expression of key cell growth genes during transitions into, and out of, the rapid growth state in glucose, while TORC1 is important for the steady-state expression of the same genes. This circuit design may enable yeast to set an exact growth rate based on the abundance of internal metabolites such as amino acids, via TORC1, but also adapt rapidly to changes in external nutrients, such as glucose, via PKA.</div>
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Integrated TORC1 and PKA signaling control the temporal activation of glucose-induced gene expression in yeast.

Integrated TORC1 and PKA signaling control the temporal activation of glucose-induced gene expression in yeast.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

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