ArticleCell metabolism2011
Regulation of yeast chronological life span by TORC1 via adaptive mitochondrial ROS signaling.
Article in Cell metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.
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Who cites it
186 citing papers in PubMed, 307 citations in OpenAlex.
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- Yeast Chronological Lifespan Model as a Tool for Screening Aging Interventions.International journal of molecular sciences · 2026Review
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- Histone methyltransferase SET-18/SMYD2-mediated activation of NADase TIR-1d/SARM1 increases mtROS to promote aging.iScience · 2026Article
- In vivo anti-aging effects of naringin, a bioflavonoid: insights from the budding yeast Saccharomyces cerevisiae as a model organism.Biogerontology · 2025Article
- Mechanisms and Strategies for Engineering Oxidative Stress Resistance inChem & bio engineering · 2025Review
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- Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole.Antioxidants (Basel, Switzerland) · 2024Review
- Ageing-dependent thiol oxidation reveals early oxidation of proteins with core proteostasis functions.Life science alliance · 2024Article
- Sit4 Genetically Interacts with Vps27 to Regulate Mitochondrial Function and Lifespan inCells · 2024Article
- Redox regulation in lifespan determination.The Journal of biological chemistry · 2024Review
- Beneficial Effects of Low-Grade Mitochondrial Stress on Metabolic Diseases and Aging.Yonsei medical journal · 2024Review
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- Sir2 and Glycerol Underlie the Pro-Longevity Effect of Quercetin during Yeast Chronological Aging.International journal of molecular sciences · 2023Article
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- Tra1 controls the transcriptional landscape of the aging cell.G3 (Bethesda, Md.) · 2023Article
126 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Here we show that yeast strains with reduced target of rapamycin (TOR) signaling have greater overall mitochondrial electron transport chain activity during growth that is efficiently coupled to ATP production. This metabolic alteration increases mitochondrial membrane potential and reactive oxygen species (ROS) production, which we propose supplies an adaptive signal during growth that extends chronological life span (CLS). In strong support of this concept, uncoupling respiration during growth or increasing expression of mitochondrial manganese superoxide dismutase significantly curtails CLS extension in tor1Δ strains, and treatment of wild-type strains with either rapamycin (to inhibit TORC1) or menadione (to generate mitochondrial ROS) during growth is sufficient to extend CLS. Finally, extension of CLS by reduced TORC1/Sch9p-mitochondrial signaling occurs independently of Rim15p and is not a function of changes in media acidification/composition. Considering the conservation of TOR-pathway effects on life span, mitochondrial ROS signaling may be an important mechanism of longevity regulation in higher organisms.
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