ArticleMolecular and cellular biology2006
Defective mitochondrial gene expression results in reactive oxygen species-mediated inhibition of respiration and reduction of yeast life span.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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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.
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Who cites it
65 citing papers in PubMed, 134 citations in OpenAlex.
- Chromatin stability safeguards mitochondrial homeostasis and restrains TORC1 signaling.PLoS genetics · 2026Article
- Chromosome duplication causes premature aging via defects in ribosome quality control.PLoS biology · 2025Article
- Proteomic and phosphoproteomic signatures of aging mouse liver.GeroScience · 2025Article
- Glucosinolates from Seed-Press Cake ofAntioxidants (Basel, Switzerland) · 2025Article
- Mechanistic insights into cisplatin-induced ototoxicity: the central role of transient receptor potential channels.Frontiers in molecular biosciences · 2025Review
- P53-dependent hypusination of eIF5A affects mitochondrial translation and senescence immune surveillance.Nature communications · 2024Article
- Premature aging in aneuploid yeast is caused in part by aneuploidy-induced defects in Ribosome Quality Control.bioRxiv : the preprint server for biology · 2024Article
- Mitochondrial Reactive Oxygen Species in Infection and Immunity.Biomolecules · 2024Review
- Glucosylglycerol and proline reverse the effects of glucose on Rhodosporidium toruloides lifespan.Archives of microbiology · 2024Article
- Exogenous glucosylglycerol and proline extend the chronological lifespan of Rhodosporidium toruloides.International microbiology : the official journal of the Spanish Society for Microbiology · 2023Article
- Glucosylglycerol Extends Chronological Lifespan of the Budding Yeast via an Increased Osmolarity Response.Indian journal of microbiology · 2023Article
- Mitochondrial Reactive Oxygen Species Elicit Acute and Chronic Itch via Transient Receptor Potential Canonical 3 Activation in Mice.Neuroscience bulletin · 2022Article
- Ehretiquinone fromOxidative medicine and cellular longevity · 2021Article
- Hair Cell Protection from Ototoxic Drugs.Neural plasticity · 2021Review
- Mitophagy Impairment Aggravates Cisplatin-Induced Ototoxicity.BioMed research international · 2021Article
- Nicotinamide, Nicotinamide Riboside and Nicotinic Acid-Emerging Roles in Replicative and Chronological Aging in Yeast.Biomolecules · 2020Review
- Cell organelles and yeast longevity: an intertwined regulation.Current genetics · 2020Review
- Mitochondria-Targeted Antioxidants for Treatment of Hearing Loss: A Systematic Review.Antioxidants (Basel, Switzerland) · 2019Review
- Proteasome lid bridges mitochondrial stress with Cdc53/Cullin1 NEDDylation status.Redox biology · 2019Article
- Mitochondria reorganization upon proliferation arrest predicts individual yeast cell fate.eLife · 2018Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondrial dysfunction causes numerous human diseases and is widely believed to be involved in aging. However, mechanisms through which compromised mitochondrial gene expression elicits the reported variety of cellular defects remain unclear. The amino-terminal domain (ATD) of yeast mitochondrial RNA polymerase is required to couple transcription to translation during expression of mitochondrial DNA-encoded oxidative phosphorylation subunits. Here we report that several ATD mutants exhibit reduced chronological life span. The most severe of these (harboring the rpo41-R129D mutation) displays imbalanced mitochondrial translation, conditional inactivation of respiration, elevated production of reactive oxygen species (ROS), and increased oxidative stress. Reduction of ROS, via overexpression of superoxide dismutase (SOD1 or SOD2 product), not only greatly extends the life span of this mutant but also increases its ability to respire. Another ATD mutant with similarly reduced respiration (rpo41-D152A/D154A) accumulates only intermediate levels of ROS and has a less severe life span defect that is not rescued by SOD. Altogether, our results provide compelling evidence for the "vicious cycle" of mitochondrial ROS production and lead us to propose that the amount of ROS generated depends on the precise nature of the mitochondrial gene expression defect and initiates a downward spiral of oxidative stress only if a critical threshold is crossed.
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Registered trials
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.