Bidirectional regulation between TORC1 and autophagy in Saccharomyces cerevisiae.
Identifieur interne : 001335 ( Main/Exploration ); précédent : 001334; suivant : 001336Bidirectional regulation between TORC1 and autophagy in Saccharomyces cerevisiae.
Auteurs : Chun-Shik Shin [Corée du Sud] ; Won-Ki HuhSource :
- Autophagy [ 1554-8635 ] ; 2011.
Descripteurs français
- KwdFr :
- Autophagie (MeSH), Azote (déficit), Facteurs de transcription (métabolisme), Mutation (génétique), Noyau de la cellule (métabolisme), Phosphorylation (MeSH), Protéines de Saccharomyces cerevisiae (métabolisme), Saccharomyces cerevisiae (cytologie), Saccharomyces cerevisiae (enzymologie), Saccharomyces cerevisiae (métabolisme), Transport des protéines (MeSH), Viabilité microbienne (MeSH).
- MESH :
- cytologie : Saccharomyces cerevisiae.
- déficit : Azote.
- enzymologie : Saccharomyces cerevisiae.
- génétique : Mutation.
- métabolisme : Facteurs de transcription, Noyau de la cellule, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- Autophagie, Phosphorylation, Transport des protéines, Viabilité microbienne.
English descriptors
- KwdEn :
- Autophagy (MeSH), Cell Nucleus (metabolism), Microbial Viability (MeSH), Mutation (genetics), Nitrogen (deficiency), Phosphorylation (MeSH), Protein Transport (MeSH), Saccharomyces cerevisiae (cytology), Saccharomyces cerevisiae (enzymology), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (metabolism), Transcription Factors (metabolism).
- MESH :
- chemical , deficiency : Nitrogen.
- cytology : Saccharomyces cerevisiae.
- enzymology : Saccharomyces cerevisiae.
- genetics : Mutation.
- metabolism : Cell Nucleus, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Transcription Factors.
- Autophagy, Microbial Viability, Phosphorylation, Protein Transport.
Abstract
It has been reported in various model organisms that autophagy and the target of rapamycin complex 1 (TORC1) signaling are strongly involved in eukaryotic cell aging and decreasing TORC1 activity extends longevity by an autophagy-dependent mechanism. Thus, to expand our knowledge of the regulation of eukaryotic cell aging, it is important to understand the relationship between TORC1 signaling and autophagy. Many researchers have shown that TORC1 represses autophagy under normal growth conditions, and TORC1 inactivation contributes to the upregulation of autophagy. However, it is poorly understood how autophagy is regulated or terminated when starvation is prolonged. Here, we report that bidirectional regulation between autophagy and TORC1 exists in the yeast Saccharomyces cerevisiae. We show that mutant cells with weak TORC1 activity maintain autophagy longer than wild-type cells, and TORC1 is partially reactivated under ongoing nitrogen starvation by an autophagy-dependent mechanism. In addition, we found that Atg13 is gradually rephosphorylated during prolonged nitrogen starvation, and the kinase activity of Atg1 is required for Atg13 rephosphorylation. Our data suggest that TORC1 can be substantially, if not fully, reactivated in an autophagy-dependent manner under ongoing starvation, and that partially reactivated TORC1 eventually plays a role in the attenuation of autophagy.
DOI: 10.4161/auto.7.8.15696
PubMed: 21490424
Affiliations:
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Research Center for Functional Cellulomics, Institute of Microbiology, Seoul National University, Seoul, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>School of Biological Sciences and Research Center for Functional Cellulomics, Institute of Microbiology, Seoul National University, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName><orgName type="university">Université nationale de Séoul</orgName></affiliation></author><author><name sortKey="Huh, Won Ki" sort="Huh, Won Ki" uniqKey="Huh W" first="Won-Ki" last="Huh">Won-Ki Huh</name></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (MeSH)</term><term>Cell 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(MeSH)</term><term>Viabilité microbienne (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Nitrogen</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Azote</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Nucleus</term><term>Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Noyau de la cellule</term><term>Protéines de Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autophagy</term><term>Microbial Viability</term><term>Phosphorylation</term><term>Protein Transport</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Phosphorylation</term><term>Transport des protéines</term><term>Viabilité microbienne</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It has been reported in various model organisms that autophagy and the target of rapamycin complex 1 (TORC1) signaling are strongly involved in eukaryotic cell aging and decreasing TORC1 activity extends longevity by an autophagy-dependent mechanism. Thus, to expand our knowledge of the regulation of eukaryotic cell aging, it is important to understand the relationship between TORC1 signaling and autophagy. Many researchers have shown that TORC1 represses autophagy under normal growth conditions, and TORC1 inactivation contributes to the upregulation of autophagy. However, it is poorly understood how autophagy is regulated or terminated when starvation is prolonged. Here, we report that bidirectional regulation between autophagy and TORC1 exists in the yeast Saccharomyces cerevisiae. We show that mutant cells with weak TORC1 activity maintain autophagy longer than wild-type cells, and TORC1 is partially reactivated under ongoing nitrogen starvation by an autophagy-dependent mechanism. In addition, we found that Atg13 is gradually rephosphorylated during prolonged nitrogen starvation, and the kinase activity of Atg1 is required for Atg13 rephosphorylation. Our data suggest that TORC1 can be substantially, if not fully, reactivated in an autophagy-dependent manner under ongoing starvation, and that partially reactivated TORC1 eventually plays a role in the attenuation of autophagy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21490424</PMID><DateCompleted><Year>2011</Year><Month>10</Month><Day>21</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>8</Issue><PubDate><Year>2011</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>Bidirectional regulation between TORC1 and autophagy in Saccharomyces cerevisiae.</ArticleTitle><Pagination><MedlinePgn>854-62</MedlinePgn></Pagination><Abstract><AbstractText>It has been reported in various model organisms that autophagy and the target of rapamycin complex 1 (TORC1) signaling are strongly involved in eukaryotic cell aging and decreasing TORC1 activity extends longevity by an autophagy-dependent mechanism. 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