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Mutations in theclk-1 gene of the nematodeCaenorhabditis elegans result in slowed development, sluggish adult behaviors, and an increased lifespan. CLK-1 is a mitochondrial polypeptide with sequence and functional conservation from human to yeast. Coq7p, theSaccharomyces cerevisiae homologue, is essential for ubiquinone (coenzyme Q or Q) synthesis and therefore respiration. However, based on assays of respiratory function, it has been reported that the primary defect in theC. elegans clk-1 mutants is not in Q biosynthesis. How do theclk-1 mutant worms have essentially normal rates of respiration, when biochemical studies in yeast suggest a Q deficiency? Nematodes are routinely fedEscherichia coli strains containing a rich supply of Q. To study the Q synthesized byC. elegans , we cultured worms on anE. coli mutant that lacks Q and found thatclk-1 mutants display early developmental arrest from eggs, or sterility emerging from dauer stage. Provision of Q-repleteE. coli rescues these defects. Lipid analysis showed thatclk-1 worms lack the nematode Q9 isoform and instead contain a large amount of a metabolite that is slightly more polar than Q9 . Theclk-1 mutants also have increased levels of Q8 , theE. coli isoform, and rhodoquinone-9. These results show that theclk-1 mutations result in Q auxotrophy evident only when Q is removed from the diet, and that the aging and developmental phenotypes previously described are consistent with altered Q levels and distribution.

A dietary source of coenzyme Q is essential for growth of long-lived Caenorhabditis elegans clk-1 mutants