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.