ArticleProceedings of the National Academy of Sciences of the United States of America2014
Deletion of conserved protein phosphatases reverses defects associated with mitochondrial DNA damage in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Potassium ion homeostasis modulates mitochondrial function.The Journal of cell biology · 2026Article
- Gene dosage adaptations to mtDNA depletion and mitochondrial protein stress in budding yeast.G3 (Bethesda, Md.) · 2024Article
- Article
- The metabolic growth limitations of petite cells lacking the mitochondrial genome.Nature metabolism · 2021Article
- LRRK2 inhibition potentiates PARP inhibitor cytotoxicity through inhibiting homologous recombination-mediated DNA double strand break repair.Clinical and translational medicine · 2021Article
- mitoXplorer, a visual data mining platform to systematically analyze and visualize mitochondrial expression dynamics and mutations.Nucleic acids research · 2020Article
- Ser/Thr protein phosphatases in fungi: structure, regulation and function.Microbial cell (Graz, Austria) · 2019Review
- Bacterial tail anchors can target to the mitochondrial outer membrane.Biology direct · 2017Article
- The ceramide-activated protein phosphatase Sit4p controls lifespan, mitochondrial function and cell cycle progression by regulating hexokinase 2 phosphorylation.Cell cycle (Georgetown, Tex.) · 2016Article
- Reduced Glucose Sensation Can Increase the Fitness of Saccharomyces cerevisiae Lacking Mitochondrial DNA.PloS one · 2016Article
- Mitochondria to nucleus signaling and the role of ceramide in its integration into the suite of cell quality control processes during aging.Ageing research reviews · 2015Review
- MitoLoc: A method for the simultaneous quantification of mitochondrial network morphology and membrane potential in single cells.Mitochondrion · 2015Article
- Vacuolar ATPase depletion affects mitochondrial ATPase function, kinetoplast dependency, and drug sensitivity in trypanosomes.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Adaptation of HepG2 cells to a steady-state reduction in the content of protein phosphatase 6 (PP6) catalytic subunit.Experimental cell research · 2015Article
- Yeast as a system for modeling mitochondrial disease mechanisms and discovering therapies.Disease models & mechanisms · 2015Review
- Activation of the pleiotropic drug resistance pathway can promote mitochondrial DNA retention by fusion-defective mitochondria in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2014Article
- The retrograde response: a conserved compensatory reaction to damage from within and from without.Progress in molecular biology and translational science · 2014Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial biogenesis is regulated by signaling pathways sensitive to extracellular conditions and to the internal environment of the cell. Therefore, treatments for disease caused by mutation of mtDNA may emerge from studies of how signal transduction pathways command mitochondrial function. We have examined the role of phosphatases under the control of the conserved α4/Tap42 protein in cells lacking a mitochondrial genome. We found that deletion of protein phosphatase 2A (PP2A) or of protein phosphatase 6 (PP6) protects cells from the reduced proliferation, mitochondrial protein import defects, lower mitochondrial electrochemical potential, and nuclear transcriptional response associated with mtDNA damage. Moreover, PP2A or PP6 deletion allows viability of a sensitized yeast strain after mtDNA loss. Interestingly, the Saccharomyces cerevisiae ortholog of the mammalian AMP-activated protein kinase was required for the full benefits of PP6 deletion and also for proliferation of otherwise wild-type cells lacking mtDNA. Our work highlights the important role that nutrient-responsive signaling pathways can play in determining the response to mitochondrial dysfunction.
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