Yeast protein expression profile during acetic acid-induced apoptosis indicates causal involvement of the TOR pathway.
Identifieur interne : 001548 ( Main/Corpus ); précédent : 001547; suivant : 001549Yeast protein expression profile during acetic acid-induced apoptosis indicates causal involvement of the TOR pathway.
Auteurs : Bruno Almeida ; Steffen Ohlmeier ; Agostinho J. Almeida ; Frank Madeo ; Cecília Leão ; Fernando Rodrigues ; Paula LudovicoSource :
- Proteomics [ 1615-9861 ] ; 2009.
English descriptors
- KwdEn :
- Acetic Acid (pharmacology), Apoptosis (drug effects), Blotting, Western (MeSH), Electrophoresis, Gel, Two-Dimensional (MeSH), Gene Expression Regulation, Fungal (drug effects), Mass Spectrometry (MeSH), Protein-Serine-Threonine Kinases (metabolism), Reactive Oxygen Species (metabolism), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , metabolism : Protein-Serine-Threonine Kinases, Reactive Oxygen Species, Saccharomyces cerevisiae Proteins.
- chemical , pharmacology : Acetic Acid.
- drug effects : Apoptosis, Gene Expression Regulation, Fungal, Saccharomyces cerevisiae, Signal Transduction.
- metabolism : Saccharomyces cerevisiae.
- Blotting, Western, Electrophoresis, Gel, Two-Dimensional, Mass Spectrometry.
Abstract
Although acetic acid has been shown to induce apoptosis in yeast, the exact apoptotic mechanisms remain unknown. Here, we studied the effects of acetic acid treatment on yeast cells by 2-DE, revealing alterations in the levels of proteins directly or indirectly linked with the target of rapamycin (TOR) pathway: amino-acid biosynthesis, transcription/translation machinery, carbohydrate metabolism, nucleotide biosynthesis, stress response, protein turnover and cell cycle. The increased levels of proteins involved in amino-acid biosynthesis presented a counteracting response to a severe intracellular amino-acid starvation induced by acetic acid. Deletion of GCN4 and GCN2 encoding key players of general amino-acid control (GAAC) system caused a higher resistance to acetic acid indicating an involvement of Gcn4p/Gcn2p in the apoptotic signaling. Involvement of the TOR pathway in acetic acid-induced apoptosis was also reflected by the higher survival rates associated to a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-negative phenotype and lower reactive oxygen species levels of Deltator1 cells. In addition, deletion mutants for several downstream mediators of the TOR pathway revealed that apoptotic signaling involves the phosphatases Pph21p and Pph22p but not Sit4p. Altogether, our results indicate that GAAC and TOR pathways (Tor1p) are involved in the signaling of acetic acid-induced apoptosis.
DOI: 10.1002/pmic.200700816
PubMed: 19137548
Links to Exploration step
pubmed:19137548Le document en format XML
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<author><name sortKey="Almeida, Bruno" sort="Almeida, Bruno" uniqKey="Almeida B" first="Bruno" last="Almeida">Bruno Almeida</name>
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<author><name sortKey="Ohlmeier, Steffen" sort="Ohlmeier, Steffen" uniqKey="Ohlmeier S" first="Steffen" last="Ohlmeier">Steffen Ohlmeier</name>
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<author><name sortKey="Almeida, Agostinho J" sort="Almeida, Agostinho J" uniqKey="Almeida A" first="Agostinho J" last="Almeida">Agostinho J. Almeida</name>
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<author><name sortKey="Madeo, Frank" sort="Madeo, Frank" uniqKey="Madeo F" first="Frank" last="Madeo">Frank Madeo</name>
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<author><name sortKey="Leao, Cecilia" sort="Leao, Cecilia" uniqKey="Leao C" first="Cecília" last="Leão">Cecília Leão</name>
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<author><name sortKey="Rodrigues, Fernando" sort="Rodrigues, Fernando" uniqKey="Rodrigues F" first="Fernando" last="Rodrigues">Fernando Rodrigues</name>
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<author><name sortKey="Ludovico, Paula" sort="Ludovico, Paula" uniqKey="Ludovico P" first="Paula" last="Ludovico">Paula Ludovico</name>
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<term>Electrophoresis, Gel, Two-Dimensional (MeSH)</term>
<term>Gene Expression Regulation, Fungal (drug effects)</term>
<term>Mass Spectrometry (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>Saccharomyces cerevisiae (drug effects)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Gene Expression Regulation, Fungal</term>
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<front><div type="abstract" xml:lang="en">Although acetic acid has been shown to induce apoptosis in yeast, the exact apoptotic mechanisms remain unknown. Here, we studied the effects of acetic acid treatment on yeast cells by 2-DE, revealing alterations in the levels of proteins directly or indirectly linked with the target of rapamycin (TOR) pathway: amino-acid biosynthesis, transcription/translation machinery, carbohydrate metabolism, nucleotide biosynthesis, stress response, protein turnover and cell cycle. The increased levels of proteins involved in amino-acid biosynthesis presented a counteracting response to a severe intracellular amino-acid starvation induced by acetic acid. Deletion of GCN4 and GCN2 encoding key players of general amino-acid control (GAAC) system caused a higher resistance to acetic acid indicating an involvement of Gcn4p/Gcn2p in the apoptotic signaling. Involvement of the TOR pathway in acetic acid-induced apoptosis was also reflected by the higher survival rates associated to a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-negative phenotype and lower reactive oxygen species levels of Deltator1 cells. In addition, deletion mutants for several downstream mediators of the TOR pathway revealed that apoptotic signaling involves the phosphatases Pph21p and Pph22p but not Sit4p. Altogether, our results indicate that GAAC and TOR pathways (Tor1p) are involved in the signaling of acetic acid-induced apoptosis.</div>
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<Abstract><AbstractText>Although acetic acid has been shown to induce apoptosis in yeast, the exact apoptotic mechanisms remain unknown. Here, we studied the effects of acetic acid treatment on yeast cells by 2-DE, revealing alterations in the levels of proteins directly or indirectly linked with the target of rapamycin (TOR) pathway: amino-acid biosynthesis, transcription/translation machinery, carbohydrate metabolism, nucleotide biosynthesis, stress response, protein turnover and cell cycle. The increased levels of proteins involved in amino-acid biosynthesis presented a counteracting response to a severe intracellular amino-acid starvation induced by acetic acid. Deletion of GCN4 and GCN2 encoding key players of general amino-acid control (GAAC) system caused a higher resistance to acetic acid indicating an involvement of Gcn4p/Gcn2p in the apoptotic signaling. Involvement of the TOR pathway in acetic acid-induced apoptosis was also reflected by the higher survival rates associated to a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-negative phenotype and lower reactive oxygen species levels of Deltator1 cells. In addition, deletion mutants for several downstream mediators of the TOR pathway revealed that apoptotic signaling involves the phosphatases Pph21p and Pph22p but not Sit4p. Altogether, our results indicate that GAAC and TOR pathways (Tor1p) are involved in the signaling of acetic acid-induced apoptosis.</AbstractText>
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