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dc.creatorJonassen, Tanya
dc.creatorLarsen, Pamela L.
dc.creatorClarke, Catherine F.
dc.date2001-01-16
dc.date2001-01-02
dc.date.accessioned2020-01-30T21:08:57Z
dc.date.available2020-01-30T21:08:57Z
dc.identifier/pmc/articles/PMC14601/
dc.identifier/pubmed/11136229
dc.identifier.urihttps://dspace.sunyconnect.suny.edu/handle/1951/71070
dc.descriptionMutations in the clk-1 gene of the nematode Caenorhabditis 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, the Saccharomyces 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 the C. elegans clk-1 mutants is not in Q biosynthesis. How do the clk-1 mutant worms have essentially normal rates of respiration, when biochemical studies in yeast suggest a Q deficiency? Nematodes are routinely fed Escherichia coli strains containing a rich supply of Q. To study the Q synthesized by C. elegans, we cultured worms on an E. coli mutant that lacks Q and found that clk-1 mutants display early developmental arrest from eggs, or sterility emerging from dauer stage. Provision of Q-replete E. coli rescues these defects. Lipid analysis showed that clk-1 worms lack the nematode Q(9) isoform and instead contain a large amount of a metabolite that is slightly more polar than Q(9). The clk-1 mutants also have increased levels of Q(8), the E. coli isoform, and rhodoquinone-9. These results show that the clk-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.
dc.languageen
dc.publisherThe National Academy of Sciences
dc.rightsCopyright © 2001, The National Academy of Sciences
dc.subjectBiological Sciences
dc.titleA dietary source of coenzyme Q is essential for growth of long-lived Caenorhabditis elegans clk-1 mutants
dc.typeText


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