The Chronological Life Span of Saccharomyces cerevisiae

AbstractDiet plays a key role in determining the longevity of the organisms since it has been demonstrated that glucose restriction increases lifespan whereas a high-glucose diet decreases it. However, the molecular basis of how diet leads to the aging process is currently unknown. We propose that the quantity of glucose that fuels respiration influences ROS generation and glutathione levels, and both chemical species impact in the aging process. Herein, we provide evidence that mutation of the gene GSH1 diminishes glutathione levels. Moreover, glutathione levels were higher with 0.5% than in 10% glucose in the gsh1Δ and WT strains. Interestingly, the chronological life span (CLS) was lowered in the gsh1Δ strain cultured with 10% glucose but not under dietary restriction. The gsh1Δ strain also showed an inhibition of the mitochondrial respiration in 0.5 and 10% of glucose but only increased the H2O2 levels under dietary restriction. These results correlate well with the GSH/GSSG ratio, which showed a decrease in gsh1Δ strain cultured with 0.5% glucose. Altogether these data indicate that glutathione has a major role in the function of electron transport chain (ETC) and is essential to maintain life span of Saccharomyces cerevisiae in 10% glucose.

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Resveratrol induces mitochondrial dysfunction and decreases chronological life span of Saccharomyces cerevisiae in a glucose-dependent manner

Journal of Bioenergetics and Biomembranes ◽

10.1007/s10863-017-9709-9 ◽

2017 ◽

Vol 49 (3) ◽

pp. 241-251 ◽

Cited By ~ 6

Author(s):

Minerva Ramos-Gomez ◽

Ivanna Karina Olivares-Marin ◽

Melina Canizal-García ◽

Juan Carlos González-Hernández ◽

Gerardo M. Nava ◽

...

Keyword(s):

Saccharomyces Cerevisiae ◽

Life Span ◽

Mitochondrial Dysfunction ◽

Dependent Manner ◽

Chronological Life Span

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Resveratrol induces mitochondrial dysfunction and decreases chronological life span of Saccharomyces cerevisiae in a glucose-dependent manner

10.1101/118307 ◽

2017 ◽

Cited By ~ 1

Author(s):

Minerva Ramos-Gomez ◽

Ivanna Karina Olivares-Marin ◽

Melina Canizal-García ◽

Juan Carlos González-Hernández ◽

Gerardo M. Nava ◽

...

Keyword(s):

Saccharomyces Cerevisiae ◽

Oxygen Consumption ◽

Life Span ◽

Mitochondrial Dysfunction ◽

Mitochondrial Membrane ◽

Exponential Phase ◽

Dependent Manner ◽

Yeast Cultures ◽

Chronological Life Span ◽

High Level

AbstractA broad range of health benefits have been attributed to resveratrol (RSV) supplementation in mammalian systems, including the increases in longevity. Nonetheless, despite the growing number of studies performed with RSV, the molecular mechanism by which it acts still remains unknown. Recently, it has been proposed that inhibition of the oxidative phosphorylation activity is the principal mechanism of RSV action. This mechanism suggests that RSV might induce mitochondrial dysfunction resulting in oxidative damage to cells with a concomitant decrease of cell viability and cellular life span. To prove this hypothesis, the chronological life span (CLS) of Saccharomyces cerevisiae was studied as it is accepted as an important model of oxidative damage and aging. In addition, oxygen consumption, mitochondrial membrane potential, and hydrogen peroxide (H2O2) release were measured in order to determine the extent of mitochondrial dysfunction. The results demonstrated that the supplementation of S. cerevisiae cultures with 100 μM RSV decreased CLS in a glucose-dependent manner. At high-level glucose, RSV supplementation increased oxygen consumption during the exponential phase yeast cultures, but inhibited it in chronologically aged yeast cultures. However, at low-level glucose, oxygen consumption was inhibited in yeast cultures in the exponential phase as well as in chronologically aged cultures. Furthermore, RSV supplementation promoted the polarization of the mitochondrial membrane in both cultures. Finally, RSV decreased the release of H2O2 with high-level glucose and increased it at low-level glucose. Altogether, this data supports the hypothesis that RSV supplementation decreases CLS as a result of mitochondrial dysfunction and this phenotype occurs in a glucose-dependent manner.

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The Budding Yeast Saccharomyces cerevisiae as a Valuable Model Organism for Investigating Anti-Aging Compounds

10.5772/intechopen.96662 ◽

2021 ◽

Author(s):

Yanni Sudiyani ◽

Muhammad Eka Prastya ◽

Roni Maryana ◽

Eka Triwahyuni ◽

Muryanto

Keyword(s):

Saccharomyces Cerevisiae ◽

Life Span ◽

Budding Yeast ◽

Model Organism ◽

Nutrient Sensing ◽

Serine Threonine Kinase ◽

Yeast Saccharomyces Cerevisiae ◽

Ethanol Acetic Acid ◽

Chronological Life Span ◽

Screening Platform

Saccharomyces cerevisiae, the budding yeast was long history as industrial baker’s yeast due to its ability to produce numerous product such as ethanol, acetate, industrial bakers etc. Interestingly, this yeast was also important tools for studying biological mechanism in eukaryotic cells including aging, autophagy, mitochondrial response etc. S. cerevisiae has arisen as a powerful chemical and genetic screening platform, due to a rapid workflow with experimental amenability and the availability of a wide range of genetic mutant libraries. Calorie restriction (CR) as the reduction of nutrients intake could promote yeast longevity through some pathways such as inhibition of nutrient sensing target of rapamycin (TOR), serine–threonine kinase (SCH9), protein adenylate cyclase (AC), protein kinase A (PKA) and ras, reduced ethanol, acetic acid and apoptotic process. In addition, CR also induces the expression of antioxidative proteins, sirtuin2 (Sir2), autophagy and induction of mitochondrial yeast adaptive response. Three methods, spotting test; chronological life span (CLS) and replicative life span (RLS) assays, have been developed to study aging in S. cerevisiae. Here, we present strategies for pharmacological anti-aging screens in yeast, discuss common pitfalls and summarize studies that have used yeast for drug discovery.

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Faculty Opinions recommendation of Life-span extension by a metacaspase in the yeast Saccharomyces cerevisiae.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718410780.793497865 ◽

2014 ◽

Author(s):

Tim Clausen ◽

Marcin Suskiewicz

Keyword(s):

Saccharomyces Cerevisiae ◽

Life Span ◽

Yeast Saccharomyces Cerevisiae ◽

Life Span Extension

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Saccharomyces cerevisiae SSD1-VConfers Longevity by a Sir2p-Independent Mechanism

Genetics ◽

10.1093/genetics/166.4.1661 ◽

2004 ◽

Vol 166 (4) ◽

pp. 1661-1672 ◽

Cited By ~ 1

Author(s):

Matt Kaeberlein ◽

Alex A Andalis ◽

Gregory B Liszt ◽

Gerald R Fink ◽

Leonard Guarente

Keyword(s):

Saccharomyces Cerevisiae ◽

Life Span ◽

Cell Cycle Progression ◽

Polymorphic Locus ◽

Cell Integrity ◽

Cycle Progression ◽

Cellular Processes ◽

Maximal Life Span ◽

Independent Mechanism ◽

Yeast Aging

AbstractThe SSD1 gene of Saccharomyces cerevisiae is a polymorphic locus that affects diverse cellular processes including cell integrity, cell cycle progression, and growth at high temperature. We show here that the SSD1-V allele is necessary for cells to achieve extremely long life span. Furthermore, addition of SSD1-V to cells can increase longevity independently of SIR2, although SIR2 is necessary for SSD1-V cells to attain maximal life span. Past studies of yeast aging have been performed in short-lived ssd1-d strain backgrounds. We propose that SSD1-V defines a previously undescribed pathway affecting cellular longevity and suggest that future studies on longevity-promoting genes should be carried out in long-lived SSD1-V strains.

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SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast

Genetics ◽

10.1093/genetics/163.1.35 ◽

2003 ◽

Vol 163 (1) ◽

pp. 35-46 ◽

Cited By ~ 3

Author(s):

Paola Fabrizio ◽

Lee-Loung Liou ◽

Vanessa N Moy ◽

Alberto Diaspro ◽

Joan Selverstone Valentine ◽

...

Keyword(s):

Life Span ◽

Stress Resistance ◽

Reversible Inactivation ◽

Life Span Extension ◽

Resistance Proteins ◽

Mitochondrial Superoxide ◽

Mitochondrial Aconitase ◽

Chronological Life Span ◽

Survival Extension ◽

Mitochondrial Superoxide Dismutase

Abstract Signal transduction pathways inactivated during periods of starvation are implicated in the regulation of longevity in organisms ranging from yeast to mammals, but the mechanisms responsible for life-span extension are poorly understood. Chronological life-span extension in S. cerevisiae cyr1 and sch9 mutants is mediated by the stress-resistance proteins Msn2/Msn4 and Rim15. Here we show that mitochondrial superoxide dismutase (Sod2) is required for survival extension in yeast. Deletion of SOD2 abolishes life-span extension in sch9Δ mutants and decreases survival in cyr1:mTn mutants. The overexpression of Sods—mitochondrial Sod2 and cytosolic CuZnSod (Sod1)—delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends survival by 30%. Deletion of the RAS2 gene, which functions upstream of CYR1, also doubles the mean life span by a mechanism that requires Msn2/4 and Sod2. These findings link mutations that extend chronological life span in S. cerevisiae to superoxide dismutases and suggest that the induction of other stress-resistance genes regulated by Msn2/4 and Rim15 is required for maximum longevity extension.

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