ArticleCell cycle (Georgetown, Tex.)2007
Cell cycle- and ribonucleotide reductase-driven changes in mtDNA copy number influence mtDNA Inheritance without compromising mitochondrial gene expression.
Article in Cell cycle (Georgetown, Tex.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- Ribonucleotide Reductase Inhibition Triggers Ferroptosis in Genetically Defined Subsets of Non-Small Cell Lung Cancer.Cancer research communications · 2026Article
- RAGE contributes to persistent sepsis-induced muscle and mitochondrial alterations.Scientific reports · 2025Article
- Inheritance bias of deletion-harbouring mtDNA in yeast: The role of copy number and intracellular selection.PLoS genetics · 2025Article
- FAM43A coordinates mtDNA replication and mitochondrial biogenesis in response to mtDNA depletion.The Journal of cell biology · 2025Article
- Gene dosage adaptations to mtDNA depletion and mitochondrial protein stress in budding yeast.G3 (Bethesda, Md.) · 2024Article
- Tolerance to replication stress requires Dun1p kinase and activation of the electron transport chain.Biochimica et biophysica acta. Molecular cell research · 2023Article
- Changes to the mtDNA copy number during yeast culture growth.Royal Society open science · 2022Article
- Mitochondrial DNA: cellular genotoxic stress sentinel.Trends in biochemical sciences · 2021Review
- The Rad53Nature communications · 2020Article
- Mitochondrial HMG-Box Containing Proteins: From Biochemical Properties to the Roles in Human Diseases.Biomolecules · 2020Review
- Elimination of rNMPs from mitochondrial DNA has no effect on its stability.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Regulation of Small Mitochondrial DNA Replicative Advantage by Ribonucleotide Reductase inG3 (Bethesda, Md.) · 2017Article
- Article
- Yeast as a system for modeling mitochondrial disease mechanisms and discovering therapies.Disease models & mechanisms · 2015Review
- Potential roles for interactions between the mitochondrial and nuclear DNA throughout the cell cycle of Schizosaccharomyces pombe.Mitochondrion · 2014Article
- Mitochondrial genomic variation associated with higher mitochondrial copy number: the Cache County Study on Memory Health and Aging.BMC bioinformatics · 2014Article
- Inheritance of the fittest mitochondria in yeast.Trends in cell biology · 2014Review
- Crosstalk between mitochondrial stress signals regulates yeast chronological lifespan.Mechanisms of ageing and development · 2014Article
- Article
- Rad53 is essential for a mitochondrial DNA inheritance checkpoint regulating G1 to S progression.The Journal of cell biology · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Most eukaryotes maintain multiple copies of mtDNA, ranging from 20-50 in yeast to as many as 10,000 in mammalian cells. The mitochondrial genome encodes essential subunits of the respiratory chain, but the number of mtDNA molecules is apparently in excess of that needed to sustain adequate respiration, as evidenced by the "threshold effect" in mitochondrial diseases. Thus, other selective pressures apparently have contributed to the universal maintenance of multiple mtDNA molecules/cell. Here we analyzed the interplay between the two pathways proposed to regulate mtDNA copy number in Saccharomyces cerevisiae, and the requirement of normal mtDNA copy number for mitochondrial gene expression, respiration, and inheritance. We provide the first direct evidence that upregulation of mtDNA can be achieved by increasing ribonucleotide reductase (RNR) activity via derepression of nuclear RNR gene transcription or elimination of allosteric-feedback regulation. Analysis of rad53 mutant strains also revealed upregulation of mtDNA copy number independent of that resulting from elevated RNR activity. We present evidence that a prolonged cell cycle allows accumulation of mtDNA in these strains. Analysis of multiple strains with increased or decreased mtDNA revealed that mechanisms are in place to prevent significant changes in mitochondrial gene expression and respiration in the face of approximately two-fold alterations in mtDNA copy number. However, depletion of mtDNA in abf2 null strains leads to defective mtDNA inheritance that is partially rescued by replenishing mtDNA via overexpression of RNR1. These results indicate that one role for multiple mtDNA copies is to ensure optimal inheritance of mtDNA during cell division.
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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.