Yeast protein expression profile during acetic acid‐induced apoptosis indicates causal involvement of the TOR pathway

Almeida, Bruno; Ohlmeier, Steffen; Almeida, Agostinho J.; Madeo, Frank; Leão, Cecı́lia; Rodrigues, Fernando; Ludovico, Paula

doi:10.1002/pmic.200700816

Cited by 85 publications

(107 citation statements)

References 40 publications

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“…It is widely believed that AA toxicity is associated with reactive oxygen species (ROS) generation and programmed cell death induction in the yeast. [8][9][10][11][12] To study and compare possible mechanisms of acetate and propionate effects on yeast, we monitored CP accumulation and the activities of selected antioxidant enzymes. These parameters are used as markers of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] It was found that WOAs were mutagenic towards the mitochondrial genome in aerobically grown baker's yeast. 2 Accumulation of acid anions in the yeast cells also resulted in energetic stress, 7 programmed cell death, [8][9][10][11][12] and inhibition of essential metabolic pathways. [13][14][15] On the other hand, baker's yeast is shown to be relatively resistant to monocarboxylic WOAs.…”

Section: Introductionmentioning

confidence: 99%

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Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

et al. 2011

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The influence of acetic and propionic acids on baker's yeast was investigated in order to expand our understanding of the effect of weak organic acid food preservatives on eukaryotic cells. Both acids decreased yeast survival in a concentration-dependent manner, but with different efficiencies. The acids inhibited the fluorescein efflux from yeast cells. The inhibition constant of fluorescein extrusion from cells treated with acetate was significantly lower in parental strain than in either PDR12 (ABC-transporter Pdr12p) or WAR1 (transcriptional factor of Pdr12p) defective mutants. The constants of inhibition by propionate were virtually the same in all strains used. Yeast exposure to acetate increased the level of oxidized proteins and the activity of antioxidant enzymes, while propionate did not change these parameters. This suggests that various mechanisms underlie the yeast toxicity by acetic and propionic acids. Our studies with mutant cells clearly indicated the involvement of Yap1p transcriptional regulator and de novo protein synthesis in superoxide dismutase up-regulation by acetate. The up-regulation of catalase was Yap1p independent. Yeast pre-incubation with low concentrations of H 2 O 2 caused cellular cross-protection against high concentrations of acetate. The results are discussed from the point of view that acetate induces a prooxidant effect in vivo, whereas propionate does not.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

et al. 2011

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“…The production of bioethanol from cellulosic Mira et al, 2010;Almeida et al, 2009;Abbot et al, 2007;Mollapour and Piper, 2007;Fernandes et al, 2003;Simõ es et al, 2006;Kawahata et al, 2006;Tenreiro et al, 2002;Tenreiro et al, 2000;Carmelo et al, 1996;Pampulha and Loureiro-Dias, 1990 Propionic acid 4.86…”

Section: Introductionmentioning

confidence: 99%

Adaptive Response and Tolerance to Weak Acids inSaccharomyces cerevisiae: A Genome-Wide View

Mira

Teixeira

Sá‐Correia

2010

OMICS: A Journal of Integrative Biology

238

277

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Weak acids are widely used as food preservatives (e.g., acetic, propionic, benzoic, and sorbic acids), herbicides (e.g., 2,4-dichlorophenoxyacetic acid), and as antimalarial (e.g., artesunic and artemisinic acids), anticancer (e.g., artesunic acid), and immunosuppressive (e.g., mycophenolic acid) drugs, among other possible applications. The understanding of the mechanisms underlying the adaptive response and resistance to these weak acids is a prerequisite to develop more effective strategies to control spoilage yeasts, and the emergence of resistant weeds, drug resistant parasites or cancer cells. Furthermore, the identification of toxicity mechanisms and resistance determinants to weak acid-based pharmaceuticals increases current knowledge on their cytotoxic effects and may lead to the identification of new drug targets. This review integrates current knowledge on the mechanisms of toxicity and tolerance to weak acid stress obtained in the model eukaryote Saccharomyces cerevisiae using genome-wide approaches and more detailed gene-by-gene analysis. The major features of the yeast response to weak acids in general, and the more specific responses and resistance mechanisms towards a specific weak acid or a group of weak acids, depending on the chemical nature of the side chain R group (R-COOH), are highlighted. The involvement of several transcriptional regulatory networks in the genomic response to different weak acids is discussed, focusing on the regulatory pathways controlled by the transcription factors Msn2p/Msn4p, War1p, Haa1p, Rim101p, and Pdr1p/Pdr3p, which are known to orchestrate weak acid stress response in yeast. The extrapolation of the knowledge gathered in yeast to other eukaryotes is also attempted.

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“…29 Interestingly, the signaling of acetic acid-induced apoptosis is linked to amino-acid metabolism as well as the TOR pathway, which both connect the nutritional situation of the cell to the aging process (see below). 30 Further external triggers: from metals to drugs. A variety of additional agents have been reported to induce an apoptotic phenotype in yeast.…”

Section: Triggering Yeast Apoptosismentioning

confidence: 99%

Apoptosis in yeast: triggers, pathways, subroutines

et al. 2010

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A cell's decision to die is controlled by a sophisticated network whose deregulation contributes to the pathogenesis of multiple diseases including neoplastic and neurodegenerative disorders. The finding, more than a decade ago, that baker's yeast (Saccharomyces cerevisiae) can undergo apoptosis uncovered the possibility to investigate this mode of programmed cell death (PCD) in a model organism that combines both technical advantages and a eukaryotic 'cell room.' Since then, numerous exogenous and endogenous triggers have been found to induce yeast apoptosis and multiple yeast orthologs of crucial metazoan apoptotic regulators have been identified and characterized at the molecular level. Such apoptosis-relevant orthologs include proteases such as the yeast caspase as well as several mitochondrial and nuclear proteins that contribute to the execution of apoptosis in a caspase-independent manner. Additionally, physiological scenarios such as aging and failed mating have been discovered to trigger apoptosis in yeast, providing a teleological interpretation of PCD affecting a unicellular organism. Due to its methodological and logistic simplicity, yeast constitutes an ideal model organism that is efficiently helping to decipher the cell death regulatory network of higher organisms, including the switches between apoptotic, autophagic, and necrotic pathways of cellular catabolism. Here, we provide an overview of the current knowledge about the apoptotic subroutine of yeast PCD and its regulation.

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Yeast protein expression profile during acetic acid‐induced apoptosis indicates causal involvement of the TOR pathway

Cited by 85 publications

References 40 publications

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

Adaptive Response and Tolerance to Weak Acids inSaccharomyces cerevisiae: A Genome-Wide View

Apoptosis in yeast: triggers, pathways, subroutines

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