ArticleMechanisms of ageing and development2014
Crosstalk between mitochondrial stress signals regulates yeast chronological lifespan.
Article in Mechanisms of ageing and development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- FAM43A coordinates mtDNA replication and mitochondrial biogenesis in response to mtDNA depletion.The Journal of cell biology · 2025Article
- Mitochondrial HMG-Box Containing Proteins: From Biochemical Properties to the Roles in Human Diseases.Biomolecules · 2020Review
- Mechanisms Through Which Some Mitochondria-Generated Metabolites Act as Second Messengers That Are Essential Contributors to the Aging Process in Eukaryotes Across Phyla.Frontiers in physiology · 2019Review
- Some Metabolites Act as Second Messengers in Yeast Chronological Aging.International journal of molecular sciences · 2018Review
- Article
- Time-course and intensity-based classifications of oxidative stresses and their potential application in biomedical, comparative and environmental research.Redox report : communications in free radical research · 2016Article
- Discovery of plant extracts that greatly delay yeast chronological aging and have different effects on longevity-defining cellular processes.Oncotarget · 2016Article
- An Energy-Independent Pro-longevity Function of Triacylglycerol in Yeast.PLoS genetics · 2016Article
- Communications between Mitochondria, the Nucleus, Vacuoles, Peroxisomes, the Endoplasmic Reticulum, the Plasma Membrane, Lipid Droplets, and the Cytosol during Yeast Chronological Aging.Frontiers in genetics · 2016Review
- A Comprehensive Analysis of Replicative Lifespan in 4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging.Cell metabolism · 2015Article
- Mechanisms by which different functional states of mitochondria define yeast longevity.International journal of molecular sciences · 2015Review
- Cell-autonomous mechanisms of chronological aging in the yeastMicrobial cell (Graz, Austria) · 2014Review
- Live longer on MARS: a yeast paradigm of mitochondrial adaptive ROS signaling in aging.Microbial cell (Graz, Austria) · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial DNA (mtDNA) exists in multiple copies per cell and is essential for oxidative phosphorylation. Depleted or mutated mtDNA promotes numerous human diseases and may contribute to aging. Reduced TORC1 signaling in the budding yeast, Saccharomyces cerevisiae, extends chronological lifespan (CLS) in part by generating a mitochondrial ROS (mtROS) signal that epigenetically alters nuclear gene expression. To address the potential requirement for mtDNA maintenance in this response, we analyzed strains lacking the mitochondrial base-excision repair enzyme Ntg1p. Extension of CLS by mtROS signaling and reduced TORC1 activity, but not caloric restriction, was abrogated in ntg1Δ strains that exhibited mtDNA depletion without defects in respiration. The DNA damage response (DDR) kinase Rad53p, which transduces pro-longevity mtROS signals, is also activated in ntg1Δ strains. Restoring mtDNA copy number alleviated Rad53p activation and re-established CLS extension following mtROS signaling, indicating that Rad53p senses mtDNA depletion directly. Finally, DDR kinases regulate nucleus-mitochondria localization dynamics of Ntg1p. From these results, we conclude that the DDR pathway senses and may regulate Ntg1p-dependent mtDNA stability. Furthermore, Rad53p senses multiple mitochondrial stresses in a hierarchical manner to elicit specific physiological outcomes, exemplified by mtDNA depletion overriding the ability of Rad53p to transduce an adaptive mtROS longevity signal.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.