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Comments on Jonassen T et al. (2003) J Biol Chem "Reproductive fitness and quinone content of Caenorhabditis elegans clk-1 mutants fed coenzyme Q isoforms of varying length." (0)
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Jonassen T, Davis DE, Larsen PL, & Clarke CF (2003). Reproductive fitness and quinone content of Caenorhabditis elegans clk-1 mutants fed coenzyme Q isoforms of varying length. J Biol Chem, 278, 51735-42. doi:10.1074/jbc.M308760200
Caenorhabditis elegans clk-1 mutants lack coenzyme Q(9) and accumulate the biosynthetic intermediate demethoxy-Q(9). A dietary source of ubiquinone (Q) is required for larval growth and development of the gonad and germ cells. We considered that uptake of the shorter Q(8) isoform present in the Escherichia coli food may contribute to the Clk phenotypes of slowed development and reduced brood size observed when the animals are fed Q-replete E. coli. To test the effect of isoprene tail length, N2 and clk-1 animals were fed E. coli engineered to produce Q(7), Q(8), Q(9), or Q(10). Wild-type nematodes showed no change in reproductive fitness regardless of the Q(n) isoform fed. clk-1(e2519) fed the Q(9) diet showed increased egg production; however, this diet did not improve reproductive fitness of the clk-1(qm30) animals. Furthermore, animals with the more severe clk-1(qm30) allele become sterile and their progeny inviable when fed Q(7)-containing bacteria. The content of Q(7) in the mitochondria of clk-1 animals was decreased relative to Q(8), suggesting less effective transport of Q(7) to the mitochondria, impaired retention, or decreased stability. Additionally, regardless of E. coli diet, clk-1(qm30) animals contain a dysfunctional dense form of mitochondria. The gonads of clk-1(qm30) worms fed Q(7)-containing food were severely shrunken and disordered. The differential fertility of clk-1 mutant nematodes fed Q isoforms may result from changes in Q localization, altered recognition by Q-binding proteins, and/or potential defects in mitochondrial function resulting from the mutant CLK-1 polypeptide itself.
