scholarly journals Yeast Life Span and its Impact on Food Fermentations

Fermentation ◽  
2019 ◽  
Vol 5 (2) ◽  
pp. 37 ◽  
Author(s):  
Aranda ◽  
Orozco ◽  
Picazo ◽  
Matallana
Keyword(s):  
Life Span ◽  
Molecular Mechanisms ◽  
Cellular Aging ◽  
Alcoholic Beverages ◽  
Successful Model ◽  
Daughter Cells ◽  
Fermentative Capacity ◽  
Yeast Biomass ◽  
Chronological Life Span ◽  
Key Factor

Yeasts are very important microorganisms for food production. The high fermentative capacity, mainly of the species of the genus Saccharomyces, is a key factor for their biotechnological use, particularly to produce alcoholic beverages. As viability and vitality are essential to ensure their correct performance in industry, this review addresses the main aspects related to the cellular aging of these fungi as their senescence impacts their proper functioning. Laboratory strains of S. cerevisiae have proven a very successful model for elucidating the molecular mechanisms that control life span. Those mechanisms are shared by all eukaryotic cells. S. cerevisiae has two models of aging, replicative and chronological. Replicative life span is measured by the number of daughter cells a mother can produce. This kind of aging is relevant when the yeast biomass is reused, as in the case of beer fermentations. Chronological life span is measured by the time cells are viable in the stationary phase, and this is relevant for batch fermentations when cells are most of the time in a non-dividing state, such as wine fermentations. The molecular causes and pathways regulating both types of aging are explained in this review.

scholarly journals Nucleolar stress causes the entry into replicative senescence in budding yeast

2018 ◽  
Author(s):  
Sandrine Morlot ◽  
Song Jia ◽  
Isabelle Léger-Silvestre ◽  
Audrey Matifas ◽  
Olivier Gadal ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Molecular Mechanisms ◽  
Replicative Senescence ◽  
Cellular Aging ◽  
Daughter Cells ◽  
Nucleolar Stress ◽  
Unique Framework ◽  
Massive Accumulation

SummaryThe accumulation of Extrachromosomal rDNA Circles (ERCs) and their asymmetric segregation upon division have been hypothesized to be responsible for replicative senescence in mother yeasts and rejuvenation in daughter cells. However, it remains unclear by which molecular mechanisms ERCs would trigger the irreversible cell cycle slow-down leading to cell death. We show that ERCs accumulation is concomitant with a nucleolar stress, characterized by a massive accumulation of pre-rRNAs in the nucleolus, leading to a loss of nucleus-to-cytoplasm ratio, decreased growth rate and cell-cycle slow-down. This nucleolar stress, observed in old mothers, is not inherited by rejuvenated daughters. Unlike WT, in the long-lived mutant fob1∆, a majority of cells is devoid of nucleolar stress and does not experience replicative senescence before death. Our study provides a unique framework to order the successive steps that govern the transition to replicative senescence and highlights the causal role of nucleolar stress in cellular aging.

scholarly journals Intragenic repeat expansions control yeast chronological aging

2019 ◽  
Author(s):  
Benjamin P Barré ◽  
Johan Hallin ◽  
Jia-Xing Yue ◽  
Karl Persson ◽  
Ekaterina Mikhalev ◽  
...  
Keyword(s):  
Life Span ◽  
Calorie Restriction ◽  
Molecular Mechanisms ◽  
Tandem Repeats ◽  
Repeat Expansion ◽  
Yeast Cells ◽  
Chronological Aging ◽  
Cellular Life ◽  
Chronological Life Span ◽  
Repeat Expansions

ABSTRACTAging varies among individuals due to both genetics and environment but the underlying molecular mechanisms remain largely unknown. Using a highly recombinedSaccharomyces cerevisiaepopulation, we found 30 distinct Quantitative Trait Loci (QTLs) that control chronological life span (CLS) in calorie rich and calorie restricted environments, and under rapamycin exposure. Calorie restriction and rapamycin extended life span in virtually all genotypes, but through different genetic variants. We tracked the two major QTLs to massive expansions of intragenic tandem repeats in the cell wall glycoproteinsFLO11andHPF1, which caused a dramatic life span shortening. Life span impairment by N-terminalHPF1repeat expansion was partially buffered by rapamycin but not by calorie restriction. TheHPF1repeat expansion shifted yeast cells from a sedentary to a buoyant state, thereby increasing their exposure to surrounding oxygen. The higher oxygenation perturbed methionine, lipid, and purine metabolism, which likely explains the life span shortening. We conclude that fast evolving intragenic repeat expansions can fundamentally change the relationship between cells and their environment with profound effects on cellular life style and longevity.

scholarly journals Vitamin E beyond Its Antioxidant Label

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 634
Author(s):  
Anca Ungurianu ◽  
Anca Zanfirescu ◽  
Georgiana Nițulescu ◽  
Denisa Margină
Keyword(s):  
Vitamin E ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Protective Effects ◽  
Cellular Effects ◽  
Inflammatory Status ◽  
Anti Cancer ◽  
Key Factor ◽  
Exciting Potential ◽  
Underlying Mechanisms

Vitamin E, comprising tocopherols and tocotrienols, is mainly known as an antioxidant. The aim of this review is to summarize the molecular mechanisms and signaling pathways linked to inflammation and malignancy modulated by its vitamers. Preclinical reports highlighted a myriad of cellular effects like modulating the synthesis of pro-inflammatory molecules and oxidative stress response, inhibiting the NF-κB pathway, regulating cell cycle, and apoptosis. Furthermore, animal-based models have shown that these molecules affect the activity of various enzymes and signaling pathways, such as MAPK, PI3K/Akt/mTOR, JAK/STAT, and NF-κB, acting as the underlying mechanisms of their reported anti-inflammatory, neuroprotective, and anti-cancer effects. In clinical settings, not all of these were proven, with reports varying considerably. Nonetheless, vitamin E was shown to improve redox and inflammatory status in healthy, diabetic, and metabolic syndrome subjects. The anti-cancer effects were inconsistent, with both pro- and anti-malignant being reported. Regarding its neuroprotective properties, several studies have shown protective effects suggesting vitamin E as a potential prevention and therapeutic (as adjuvant) tool. However, source and dosage greatly influence the observed effects, with bioavailability seemingly a key factor in obtaining the preferred outcome. We conclude that this group of molecules presents exciting potential for the prevention and treatment of diseases with an inflammatory, redox, or malignant component.

SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 35-46 ◽  
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.

Ecl1 is a zinc-binding protein involved in the zinc-limitation-dependent extension of chronological life span in fission yeast

2017 ◽  
Vol 292 (2) ◽  
pp. 475-481 ◽  
Author(s):  
Takafumi Shimasaki ◽  
Hokuto Ohtsuka ◽  
Chikako Naito ◽  
Kenko Azuma ◽  
Takeshi Tenno ◽  
...  
Keyword(s):  
Life Span ◽  
Fission Yeast ◽  
Binding Protein ◽  
Zinc Binding ◽  
Chronological Life Span

scholarly journals The roles and mechanisms of hypoxia in liver fibrosis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingyao Cai ◽  
Min Hu ◽  
Zhiyang Chen ◽  
Zeng Ling
Keyword(s):  
Quality Of Life ◽  
Liver Fibrosis ◽  
Theoretical Basis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Clinical Intervention ◽  
Chronic Liver Injury ◽  
Key Factor

AbstractLiver fibrosis occurs in response to any etiology of chronic liver injury. Lack of appropriate clinical intervention will lead to liver cirrhosis or hepatocellular carcinoma (HCC), seriously affecting the quality of life of patients, but the current clinical treatments of liver fibrosis have not been developed yet. Recent studies have shown that hypoxia is a key factor promoting the progression of liver fibrosis. Hypoxia can cause liver fibrosis. Liver fibrosis can, in turn, profoundly further deepen the degree of hypoxia. Therefore, exploring the role of hypoxia in liver fibrosis will help to further understand the process of liver fibrosis, and provide the theoretical basis for its diagnosis and treatment, which is of great significance to avoid further deterioration of liver diseases and protect the life and health of patients. This review highlights the recent advances in cellular and molecular mechanisms of hypoxia in developments of liver fibrosis.

scholarly journals The Rho-family GTPase OsRac1 controls rice grain size and yield by regulating cell division

2019 ◽  
Vol 116 (32) ◽  
pp. 16121-16126 ◽  
Author(s):  
Ying Zhang ◽  
Yan Xiong ◽  
Renyi Liu ◽  
Hong-Wei Xue ◽  
Zhenbiao Yang
Keyword(s):  
Grain Size ◽  
Cell Division ◽  
Grain Yield ◽  
Molecular Mechanisms ◽  
Grain Filling ◽  
High Yield ◽  
Rice Grain ◽  
Rop Gtpase ◽  
Key Factor ◽  
Grain Width

Grain size is a key factor for determining grain yield in crops and is a target trait for both domestication and breeding, yet the mechanisms underlying the regulation of grain size are largely unclear. Here we show that the grain size and yield of rice (Oryza sativa) is positively regulated by ROP GTPase (Rho-like GTPase from plants), a versatile molecular switch modulating plant growth, development, and responses to the environment. Overexpression of rice OsRac1ROP not only increases cell numbers, resulting in a larger spikelet hull, but also accelerates grain filling rate, causing greater grain width and weight. As a result, OsRac1 overexpression improves grain yield in O. sativa by nearly 16%. In contrast, down-regulation or deletion of OsRac1 causes the opposite effects. RNA-seq and cell cycle analyses suggest that OsRac1 promotes cell division. Interestingly, OsRac1 interacts with and regulates the phosphorylation level of OsMAPK6, which is known to regulate cell division and grain size in rice. Thus, our findings suggest OsRac1 modulates rice grain size and yield by influencing cell division. This study provides insights into the molecular mechanisms underlying the control of rice grain size and suggests that OsRac1 could serve as a potential target gene for breeding high-yield crops.

scholarly journals Daughter cells of Saccharomyces cerevisiae from old mothers display a reduced life span.

1994 ◽  
Vol 127 (6) ◽  
pp. 1985-1993 ◽  
Author(s):  
B K Kennedy ◽  
N R Austriaco ◽  
L Guarente
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Daughter Cell ◽  
Young Mothers ◽  
Young Mother ◽  
Yeast Saccharomyces Cerevisiae ◽  
Daughter Cells ◽  
Per Se ◽  
Mother Cells ◽  
Maximum Occurrence

The yeast Saccharomyces cerevisiae typically divides asymmetrically to give a large mother cell and a smaller daughter cell. As mother cells become old, they enlarge and produce daughter cells that are larger than daughters derived from young mother cells. We found that occasional daughter cells were indistinguishable in size from their mothers, giving rise to a symmetric division. The frequency of symmetric divisions became greater as mother cells aged and reached a maximum occurrence of 30% in mothers undergoing their last cell division. Symmetric divisions occurred similarly in rad9 and ste12 mutants. Strikingly, daughters from old mothers, whether they arose from symmetric divisions or not, displayed reduced life spans relative to daughters from young mothers. Because daughters from old mothers were larger than daughters from young mothers, we investigated whether an increased size per se shortened life span and found that it did not. These findings are consistent with a model for aging that invokes a senescence substance which accumulates in old mother cells and is inherited by their daughters.

Mutagenicity, Metabolism, and DNA Interactions of Urethane

1990 ◽  
Vol 6 (1) ◽  
pp. 71-108 ◽  
Author(s):  
Rene E. Sotomayor ◽  
Thomas F.X. Collins
Keyword(s):  
Molecular Mechanisms ◽  
Case Reports ◽  
The Body ◽  
Alcoholic Beverages ◽  
Fermented Foods ◽  
X Rays ◽  
Spermatogenic Cells ◽  
Dna Interactions ◽  
Specific Locus ◽  
Vinyl Carbamate

Urethane, a known animal carcinogen, has been the subject of intensive research efforts spanning 40 years. Recent concerns have focused on the presence of urethane in a variety of fermented foods and alcoholic beverages, although no epidemiological studies or human case reports have been published. Much information is available about the mutagenesis, metabolism, and DNA interactions of urethane in experimental systems. Urethane is generally not mutagenic in bacteria although in some instances it acts as a weak mutagen. Urethane is not mutagenic in Neurospora but is weakly mutagenic in Saccharomyces. Drosophila appear to be the only organisms that consistently give positive mutagenic results with urethane, but its mutagenicity is weak and in many cases shows no clear dose dependence. Urethane is a good clastogen in mammalian somatic cells in vivo, but it shows variable results with cells in vitro. It efficiently induces sister chromatid exchanges in a variety of cells. Mammalian spermatogenic cells are insensitive to the induction of specific locus and dominant lethal mutations by urethane. Mutational synergism has been reported to occur between ethyl methanesulfonate and urethane when administered two generations apart, and some investigators have suggested possible synergism for cancer-causing mutations in mice exposed to X-rays and urethane one generation apart. These studies are controversial and have not been confirmed. Studies on the induction of cancer-causing dominant mutations by urethane are at variance with results from extensive studies with the specific locus test in mice. Urethane studies with the unscheduled DNA synthesis assay in mouse spermatogenic cells and with the sperm abnormality test have given negative results. Urethane is rapidly and evenly distributed in the body. The rate of elimination of urethane from plasma is a saturable process and varies according to the strain and age of the animal. Recent studies have concentrated on the effect of ethanol on urethane metabolism. At concentrations similar to those in wine, ethanol inhibits the tissue distribution of urethane in mice. These results are important because they suggest a lower carcinogenic/mutagenic risk than expected from exposure to urethane in alcoholic beverages. Although research on the metabolic activation of urethane has been extensive, no conclusive results have been obtained about its active metabolite, at one time thought to be N-hydroxyurethane. More recently, it has been postulated that urethane is actived to vinyl carbamate and that this metabolite is capable of reacting with DNA. Vinyl carbamate is more carcinogenic and more mutagenic than the parental compound, but despite intensive efforts it has not been identified as a metabolite in animals treated with urethane. Urethane binding to DNA appears to correlate well with tissue susceptibility to cancer. Various studies have attempted to elucidate the molecular nature of the bound molecule and the binding site. Some results have indicated the formation of a single DNA adduct, 7-(2-oxoethyl)guanine. This adduct may isomerize to O6,7-(1'-hydroxyethano)guanine, which might be more mutagenic than the 2-oxoethyl adduct; however, this possibility seems unlikely. Despite extensive research, urethane's metabolism and molecular mechanisms of mutation are still not clearly understood.

scholarly journals Antioxidant Responses and Gene Expression in Bermudagrass under Cold Stress

2014 ◽  
Vol 139 (6) ◽  
pp. 699-705 ◽  
Author(s):  
Jibiao Fan ◽  
Jing Ren ◽  
Weixi Zhu ◽  
Erick Amombo ◽  
Jinmin Fu ◽  
...  
Keyword(s):  
Cold Stress ◽  
Molecular Mechanisms ◽  
Cynodon Dactylon ◽  
Sugar Content ◽  
Soluble Sugar ◽  
Molecular Alteration ◽  
Antioxidant Genes ◽  
Dramatic Decline ◽  
Malondialdehyde Content ◽  
Key Factor

Cold stress is a key factor limiting resource use in bermudagrass (Cynodon dactylon). Under cold stress, bermudagrass growth is severely inhibited and the leaves undergo chlorosis. Therefore, rigorous investigation on the physiological and molecular mechanisms of cold stress in this turf species is urgent. The objective of this study was to investigate the physiological and molecular alteration in wild bermudagrass under cold stress, particularly the changes of transpiration rate, soluble sugar content, enzyme activities, and expression of antioxidant genes. Wild bermudagrass (C. dactylon) was planted in plastic pots (each 10 cm tall and 8 cm in diameter) filled with matrix (brown coal soil:sand 1:1) and treated with 4 °C in a growth chamber. The results displayed a dramatic decline in the growth and transpiration rates of the wild bermudagrass under 4 °C temperature. Simultaneously, cold severely destabilized the cell membrane as indicated by increased malondialdehyde content and electrolyte leakage value. Superoxide dismutase and peroxidase activities were higher in the cold regime than the control. The expression of antioxidant genes including MnSOD, Cu/ZnSOD, POD, and APX was vividly up-regulated after cold stress. In summary, our results contributed to the understanding of the role of the antioxidant system in bermudagrass’ response to cold.

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