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Induction of triacylglycerol synthesis in yeast by cell cycle arrest.

Identifieur interne : 000320 ( Main/Exploration ); précédent : 000319; suivant : 000321

Induction of triacylglycerol synthesis in yeast by cell cycle arrest.

Auteurs : Juliana B. Madeira ; Gabriel S. Matos ; Laryssa S. Messias ; Bruno L. Bozaquel-Morais ; Claudio A. Masuda ; Monica Montero-Lomeli

Source :

RBID : pubmed:30985885

Descripteurs français

English descriptors

Abstract

In this study, we found that cell cycle arrest induced by alpha-factor mating pheromone (G1), hydroxyurea (S) or nocodazole (G2/M) was associated to increased lipid droplet (LD) content. To identify novel cell cycle genes involved in LD homeostasis, we screened a deletion library for strains with altered LD levels. Among the mutants related to mitotic cell cycle, we found 24 hits that displayed a significantly higher LD content. Ontology mapping showed that neither a biological process nor a specific cell cycle phase was enriched among the hits. We decided to further study the role of SWI4 on LD homeostasis as it is involved in G1/S transition, a stage where lipolysis is active. The high LD content of swi4Δ mutant was not due to inhibition of lipolysis, but due to an increase in triacylglycerol (TAG) synthesis. In addition, deletion of the AMP kinase gene SNF1 or inhibition of TORC1 activity, both known regulators of LD homeostasis, further increased the LD content of a swi4Δ mutant. These findings highlight a role of the cell cycle regulator SWI4 in the coordination of lipid metabolism which is independent of the TORC1 and SNF1/AMPK pathways.

DOI: 10.1093/femsyr/foz030
PubMed: 30985885


Affiliations:


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


Le document en format XML

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<term>Cell Cycle Checkpoints (MeSH)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>Gene Deletion (MeSH)</term>
<term>Gene Expression Regulation, Fungal (MeSH)</term>
<term>Homeostasis (MeSH)</term>
<term>Lipid Droplets (metabolism)</term>
<term>Mutation (MeSH)</term>
<term>Promoter Regions, Genetic (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (antagonists & inhibitors)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Transcription Factors (antagonists & inhibitors)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
<term>Transcription, Genetic (MeSH)</term>
<term>Triglycerides (biosynthesis)</term>
</keywords>
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<term>Délétion de gène (MeSH)</term>
<term>Facteurs de transcription (antagonistes et inhibiteurs)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Gouttelettes lipidiques (métabolisme)</term>
<term>Homéostasie (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Points de contrôle du cycle cellulaire (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (antagonistes et inhibiteurs)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Régions promotrices (génétique) (MeSH)</term>
<term>Régulation de l'expression des gènes fongiques (MeSH)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Transcription génétique (MeSH)</term>
<term>Triglycéride (biosynthèse)</term>
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<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en">
<term>Saccharomyces cerevisiae Proteins</term>
<term>Transcription Factors</term>
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<term>Protein-Serine-Threonine Kinases</term>
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<term>Transcription Factors</term>
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<term>Protéines de Saccharomyces cerevisiae</term>
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<term>Triglycéride</term>
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<term>Saccharomyces cerevisiae</term>
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<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines de liaison à l'ADN</term>
<term>Saccharomyces cerevisiae</term>
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<term>Lipid Droplets</term>
<term>Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>Transcription Factors</term>
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<term>Mutation</term>
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<term>Mutation</term>
<term>Points de contrôle du cycle cellulaire</term>
<term>Régions promotrices (génétique)</term>
<term>Régulation de l'expression des gènes fongiques</term>
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<div type="abstract" xml:lang="en">In this study, we found that cell cycle arrest induced by alpha-factor mating pheromone (G1), hydroxyurea (S) or nocodazole (G2/M) was associated to increased lipid droplet (LD) content. To identify novel cell cycle genes involved in LD homeostasis, we screened a deletion library for strains with altered LD levels. Among the mutants related to mitotic cell cycle, we found 24 hits that displayed a significantly higher LD content. Ontology mapping showed that neither a biological process nor a specific cell cycle phase was enriched among the hits. We decided to further study the role of SWI4 on LD homeostasis as it is involved in G1/S transition, a stage where lipolysis is active. The high LD content of swi4Δ mutant was not due to inhibition of lipolysis, but due to an increase in triacylglycerol (TAG) synthesis. In addition, deletion of the AMP kinase gene SNF1 or inhibition of TORC1 activity, both known regulators of LD homeostasis, further increased the LD content of a swi4Δ mutant. These findings highlight a role of the cell cycle regulator SWI4 in the coordination of lipid metabolism which is independent of the TORC1 and SNF1/AMPK pathways.</div>
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<AbstractText>In this study, we found that cell cycle arrest induced by alpha-factor mating pheromone (G1), hydroxyurea (S) or nocodazole (G2/M) was associated to increased lipid droplet (LD) content. To identify novel cell cycle genes involved in LD homeostasis, we screened a deletion library for strains with altered LD levels. Among the mutants related to mitotic cell cycle, we found 24 hits that displayed a significantly higher LD content. Ontology mapping showed that neither a biological process nor a specific cell cycle phase was enriched among the hits. We decided to further study the role of SWI4 on LD homeostasis as it is involved in G1/S transition, a stage where lipolysis is active. The high LD content of swi4Δ mutant was not due to inhibition of lipolysis, but due to an increase in triacylglycerol (TAG) synthesis. In addition, deletion of the AMP kinase gene SNF1 or inhibition of TORC1 activity, both known regulators of LD homeostasis, further increased the LD content of a swi4Δ mutant. These findings highlight a role of the cell cycle regulator SWI4 in the coordination of lipid metabolism which is independent of the TORC1 and SNF1/AMPK pathways.</AbstractText>
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<Keyword MajorTopicYN="Y">Sucrose nonf-fermenting protein kinase (SNF1)</Keyword>
<Keyword MajorTopicYN="Y">Swi4/Swi6 binding factor (SBF) transcription complex</Keyword>
<Keyword MajorTopicYN="Y">Target of rapamycin complex 1 (TORC1)</Keyword>
<Keyword MajorTopicYN="Y">Triacylglycerol</Keyword>
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<name sortKey="Madeira, Juliana B" sort="Madeira, Juliana B" uniqKey="Madeira J" first="Juliana B" last="Madeira">Juliana B. Madeira</name>
<name sortKey="Masuda, Claudio A" sort="Masuda, Claudio A" uniqKey="Masuda C" first="Claudio A" last="Masuda">Claudio A. Masuda</name>
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