ArticlePLoS genetics2016
Chronological Lifespan in Yeast Is Dependent on the Accumulation of Storage Carbohydrates Mediated by Yak1, Mck1 and Rim15 Kinases.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Pooled it
- Chromosome duplication causes premature aging via defects in ribosome quality control.PLoS biology · 2025Article
- The small GTPase Rho5-Yet another player in yeast glucose signaling.PLoS genetics · 2025Article
- In vivo anti-aging effects of naringin, a bioflavonoid: insights from the budding yeast Saccharomyces cerevisiae as a model organism.Biogerontology · 2025Article
- The Yeast Gsk-3 Kinase Mck1 Is Necessary for Cell Wall Remodeling in Glucose-Starved and Cell Wall-Stressed Cells.International journal of molecular sciences · 2025Article
- Glucosinolates from Seed-Press Cake ofAntioxidants (Basel, Switzerland) · 2025Article
- Premature aging in aneuploid yeast is caused in part by aneuploidy-induced defects in Ribosome Quality Control.bioRxiv : the preprint server for biology · 2024Article
- Sit4 Genetically Interacts with Vps27 to Regulate Mitochondrial Function and Lifespan inCells · 2024Article
- Novel Roles of the Greatwall Kinase Rim15 in Yeast Oxidative Stress Tolerance through Mediating Antioxidant Systems and Transcriptional Regulation.Antioxidants (Basel, Switzerland) · 2024Article
- Mitochondria complex I deficiency in Candida albicans arrests the cell cycle at S phase through suppressive TOR and PKA pathways.FEMS yeast research · 2024Article
- TheAging · 2023Article
- Article
- Sir2 and Glycerol Underlie the Pro-Longevity Effect of Quercetin during Yeast Chronological Aging.International journal of molecular sciences · 2023Article
- The Yeast Protein Kinase Sch9 Functions as a Central Nutrient-Responsive Hub That Calibrates Metabolic and Stress-Related Responses.Journal of fungi (Basel, Switzerland) · 2023Review
- Review
- Article
- The Lipid Profile of theJournal of fungi (Basel, Switzerland) · 2022Article
- The role of NAD and NAD precursors on longevity and lifespan modulation in the budding yeast, Saccharomyces cerevisiae.Biogerontology · 2022Review
- Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast.Oncotarget · 2022Article
- Cyclin C-Cdk8 Kinase Phosphorylation of Rim15 Prevents the Aberrant Activation of Stress Response Genes.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Upon starvation for glucose or any other macronutrient, yeast cells exit from the mitotic cell cycle and acquire a set of characteristics that are specific to quiescent cells to ensure longevity. Little is known about the molecular determinants that orchestrate quiescence entry and lifespan extension. Using starvation-specific gene reporters, we screened a subset of the yeast deletion library representing the genes encoding 'signaling' proteins. Apart from the previously characterised Rim15, Mck1 and Yak1 kinases, the SNF1/AMPK complex, the cell wall integrity pathway and a number of cell cycle regulators were shown to be necessary for proper quiescence establishment and for extension of chronological lifespan (CLS), suggesting that entry into quiescence requires the integration of starvation signals transmitted via multiple signaling pathways. The CLS of these signaling mutants, and those of the single, double and triple mutants of RIM15, YAK1 and MCK1 correlates well with the amount of storage carbohydrates but poorly with transition-phase cell cycle status. Combined removal of the glycogen and trehalose biosynthetic genes, especially GSY2 and TPS1, nearly abolishes the accumulation of storage carbohydrates and severely reduces CLS. Concurrent overexpression of GSY2 and TSL1 or supplementation of trehalose to the growth medium ameliorates the severe CLS defects displayed by the signaling mutants (rim15Δyak1Δ or rim15Δmck1Δ). Furthermore, we reveal that the levels of intracellular reactive oxygen species are cooperatively controlled by Yak1, Rim15 and Mck1, and the three kinases mediate the TOR1-regulated accumulation of storage carbohydrates and CLS extension. Our data support the hypothesis that metabolic reprogramming to accumulate energy stores and the activation of anti-oxidant defence systems are coordinated by Yak1, Rim15 and Mck1 kinases to ensure quiescence entry and lifespan extension in yeast.
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Registered trials
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