ArticleCell reports2022
Deficiency of the RNA-binding protein Cth2 extends yeast replicative lifespan by alleviating its repressive effects on mitochondrial function.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Overexpression of Ssd1 and calorie restriction extend yeast replicative lifespan by preventing deleterious age-dependent iron uptake.bioRxiv : the preprint server for biology · 2025Article
- A single-cell resolved genotype-phenotype map using genome-wide genetic and environmental perturbations.Nature communications · 2025Article
- Optimization of the culture medium for an iron-sensitive oleaginous yeast, Rhodotorula toruloides NBRC 0559, through functional iron deficiency.FEMS yeast research · 2025Article
- Lifespan regulation by targeting heme signaling in yeast.GeroScience · 2024Article
- Ribosome profiling reveals the role of yeast RNA-binding proteins Cth1 and Cth2 in translational regulation.iScience · 2024Article
- Lifespan regulation by targeting heme signaling in yeast.bioRxiv : the preprint server for biology · 2024Article
- Iron Homeostatic Regulation in Saccharomyces cerevisiae: Introduction to a Computational Modeling Method.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Dietary change without caloric restriction maintains a youthful profile in ageing yeast.PLoS biology · 2023Article
- Iron Limitation Restores Autophagy and Increases Lifespan in the Yeast Model of Niemann-Pick Type C1.International journal of molecular sciences · 2023Article
- The polyHIS Tract of Yeast AMPK Coordinates Carbon Metabolism with Iron Availability.International journal of molecular sciences · 2023Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Iron dyshomeostasis contributes to aging, but little information is available about the molecular mechanisms. Here, we provide evidence that in Saccharomyces cerevisiae, aging is associated with altered expression of genes involved in iron homeostasis. We further demonstrate that defects in the conserved mRNA-binding protein Cth2, which controls stability and translation of mRNAs encoding iron-containing proteins, increase lifespan by alleviating its repressive effects on mitochondrial function. Mutation of the conserved cysteine residue in Cth2 that inhibits its RNA-binding activity is sufficient to confer longevity, whereas Cth2 gain of function shortens replicative lifespan. Consistent with its function in RNA degradation, Cth2 deficiency relieves Cth2-mediated post-transcriptional repression of nuclear-encoded components of the electron transport chain. Our findings uncover a major role of the RNA-binding protein Cth2 in the regulation of lifespan and suggest that modulation of iron starvation signaling can serve as a target for potential aging interventions.
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