ArticleScientific reports2017
A single biochemical activity underlies the pleiotropy of the aging-related protein CLK-1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Modulating Ubiquinone Biosynthesis Rescues Mitochondrial Dysfunction by Genetic Interaction in a Phosphatidylethanolamine (PE)-Deficient Disease Model.Antioxidants (Basel, Switzerland) · 2026Article
- Stress responses and dynamic equilibrium: Key determinants of aging in thebioRxiv : the preprint server for biology · 2025Article
- Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels inAntioxidants (Basel, Switzerland) · 2025Review
- Understanding coenzyme Q.Physiological reviews · 2024Review
- Cellular oxidants and the proteostasis network: balance between activation and destruction.Trends in biochemical sciences · 2024Review
- A ubiquinone precursor analogue does not clearly increase the growth rate ofmicroPublication biology · 2024Article
- Novel Homozygous Variant inNeurology. Genetics · 2023Article
- Mitochondrial dysfunction, aging, and the mitochondrial unfolded protein response in Caenorhabditis elegans.Genetics · 2022Review
- Structure and functionality of a multimeric human COQ7:COQ9 complex.Molecular cell · 2022Article
- A novelMolecular genetics and metabolism reports · 2022Article
- Mechanisms and Therapeutic Effects of Benzoquinone Ring Analogs in Primary CoQ Deficiencies.Antioxidants (Basel, Switzerland) · 2022Review
- Coenzyme Q at the Hinge of Health and Metabolic Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Elevated mitochondrial DNA copy number found in ubiquinone-deficient clk-1 mutants is not rescued by ubiquinone precursor 2-4-dihydroxybenzoate.Mitochondrion · 2021Article
- Targeting metabolic pathways for extension of lifespan and healthspan across multiple species.Ageing research reviews · 2020Review
- Decoding the rosetta stone of mitonuclear communication.Pharmacological research · 2020Review
- ADCK4 Deficiency Destabilizes the Coenzyme Q Complex, Which Is Rescued by 2,4-Dihydroxybenzoic Acid Treatment.Journal of the American Society of Nephrology : JASN · 2020Article
- Reduction in the levels of CoQ biosynthetic proteins is related to an increase in lifespan without evidence of hepatic mitohormesis.Scientific reports · 2018Article
- Mitochondrial ubiquinone-mediated longevity is marked by reduced cytoplasmic mRNA translation.Life science alliance · 2018Article
- The Impact of Aging on Cardio and Cerebrovascular Diseases.International journal of molecular sciences · 2018Review
- Cell Biology of the Mitochondrion.Genetics · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Caenorhabditis elegans clk-1 gene and the orthologous mouse gene Mclk1 encode a mitochondrial hydroxylase that is necessary for the biosynthesis of ubiquinone (UQ). Mutations in these genes produce broadly pleiotropic phenotypes in both species, including a lengthening of animal lifespan. A number of features of the C. elegans clk-1 mutants, including a maternal effect, particularly extensive pleiotropy, as well as unexplained differences between alleles have suggested that CLK-1/MCLK1 might have additional functions besides that in UQ biosynthesis. In addition, a recent study suggested that a cryptic nuclear localization signal could lead to nuclear localization in cultured mammalian cell lines. Here, by using immunohistochemical techniques in worms and purification techniques in mammalian cells, we failed to detect any nuclear enrichment of the MCLK1 or CLK-1 proteins and any biological activity of a C. elegans CLK-1 protein devoid of a mitochondrial localization sequence. In addition, and most importantly, by pharmacologically restoring UQ biosynthesis in clk-1 null mutants we show that loss of UQ biosynthesis is responsible for all phenotypes resulting from loss of CLK-1, including behavioral phenotypes, altered expression of mitochondrial quality control genes, and lifespan.
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