ArticleMolecular and cellular biology2006
Uncoupling the pleiotropic phenotypes of clk-1 with tRNA missense suppressors in Caenorhabditis elegans.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
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- Mitochondrial dysfunction, aging, and the mitochondrial unfolded protein response in Caenorhabditis elegans.Genetics · 2022Review
- A novelMolecular genetics and metabolism reports · 2022Article
- Minimal mitochondrial respiration is required to prevent cell death by inhibition of mTOR signaling in CoQ-deficient cells.Cell death discovery · 2021Article
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- Pathogenicity of two COQ7 mutations and responses to 2,4-dihydroxybenzoate bypass treatment.Journal of cellular and molecular medicine · 2017Article
- A single biochemical activity underlies the pleiotropy of the aging-related protein CLK-1.Scientific reports · 2017Article
- A Select Subset of Electron Transport Chain Genes Associated with Optic Atrophy Link Mitochondria to Axon Regeneration inFrontiers in neuroscience · 2017Article
- The mitochondrial unfolded protein response activator ATFS-1 protects cells from inhibition of the mevalonate pathway.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- A mitochondrial superoxide signal triggers increased longevity in Caenorhabditis elegans.PLoS biology · 2010Article
- Reversal of the mitochondrial phenotype and slow development of oxidative biomarkers of aging in long-lived Mclk1+/- mice.The Journal of biological chemistry · 2009Article
- The effect of different ubiquinones on lifespan in Caenorhabditis elegans.Mechanisms of ageing and development · 2009Article
- A regulated response to impaired respiration slows behavioral rates and increases lifespan in Caenorhabditis elegans.PLoS genetics · 2009Article
- Early mitochondrial dysfunction in long-lived Mclk1+/- mice.The Journal of biological chemistry · 2008Article
- Article
- Genetic evidence for an interaction of the UbiG O-methyltransferase with UbiX in Escherichia coli coenzyme Q biosynthesis.Journal of bacteriology · 2006Article
- The role of DMQ(9) in the long-lived mutant clk-1.Mechanisms of ageing and developmentArticle
- Molecular genetics of ubiquinone biosynthesis in animals.Critical reviews in biochemistry and molecular biologyReview
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
clk-1 encodes a demethoxyubiquinone (DMQ) hydroxylase that is necessary for ubiquinone biosynthesis. When Caenorhabditis elegans clk-1 mutants are grown on bacteria that synthesize ubiquinone (UQ), they are viable but have a pleiotropic phenotype that includes slowed development, behaviors, and aging. However, when grown on UQ-deficient bacteria, the mutants arrest development transiently before growing up to become sterile adults. We identified nine suppressors of the missense mutation clk-1(e2519), which harbors a Glu-to-Lys substitution. All suppress the mutant phenotypes on both UQ-replete and UQ-deficient bacteria. However, each mutant suppresses a different subset of phenotypes, indicating that most phenotypes can be uncoupled from each other. In addition, all suppressors restore the ability to synthesize exceedingly small amounts of UQ, although they still accumulate the precursor DMQ, suggesting that the presence of DMQ is not responsible for the Clk-1 phenotypes. We cloned six of the suppressors, and all encode tRNA(Glu) genes whose anticodons are altered to read the substituted Lys codon of clk-1(e2519). To our knowledge, these suppressors represent the first missense suppressors identified in any metazoan. The pattern of suppression we observe suggests that the individual members of the tRNA(Glu) family are expressed in different tissues and at different levels.
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