ArticleMitochondrion2021
Elevated mitochondrial DNA copy number found in ubiquinone-deficient clk-1 mutants is not rescued by ubiquinone precursor 2-4-dihydroxybenzoate.
Article in Mitochondrion, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Effects of mating system and adaptedness on the evolution of fitness and mtDNA copy number in mitonuclear mismatched C. elegans.Heredity · 2025Article
- Article
- Mitochondrial Factors in the Cell Nucleus.International journal of molecular sciences · 2023Review
- Structure and functionality of a multimeric human COQ7:COQ9 complex.Molecular cell · 2022Article
- Dysregulation of iron homeostasis and methamphetamine reward behaviors in Clk1-deficient mice.Acta pharmacologica Sinica · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Inside mitochondria reside semi-autonomous genomes, called mtDNA. mtDNA is multi-copy per cell and mtDNA copy number can vary from hundreds to thousands of copies per cell. The variability of mtDNA copy number between tissues, combined with the lack of variability of copy number within a tissue, suggest a homeostatic copy number regulation mechanism. Mutations in the gene encoding the Caenorhabditis elegans hydroxylase, CLK-1, result in elevated mtDNA. CLK-1's canonical role in ubiquinone biosynthesis results in clk-1 mutants lacking ubiquinone. Importantly, clk-1 mutants also exhibit slowed biological timing phenotypes (pharyngeal pumping, defecation, development) and an activated stress response (UPR
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