Assessing the Effects of a Coenzyme Q Deficient Escherichia coli Diet in Wild-type Caenorhabditis elegans and coq-3 Gene Mutant Caenorhabditis elegans Applications for Mitochondrial Disorder Studies and Probiotics

Coenzyme Q (ubiquinone or Q) is a crucial component of the cellular energy-generating electron transport chain in the mitochondria. Q is a redox-active lipid that ferries electrons provided by NADH at complex I and succinate at complex II to complex III, and is active in the Q-cycle in complex III. This important lipid plays the part of antioxidant in various biological membranes and via its reduction of oxidized alpha-tocopherol.;Living systems harboring mutations in Q biosynthesis present a variable series of phenotypes. In the model nematode C. elegans, phenotypes depend on the coq gene affected. The coq-3 mutant worms, for instance, behave differently than the other coq mutant worms when fed a Q-deficient E. coli diet. These animals have an extended life span on this food source, compared to wild-type animals fed a similar diet. However, both coq-3 mutant strains are sterile and fail to develop reproductive tissue on the Q-less diet. The results of coq-3 mutation in C. elegans are further explored in Chapter two of this dissertation.;Feeding wild-type worms a Q-less E. coli diet also increases life span. The reason for this life span extension is not due to the lack of Q per se in the bacteria. Instead, Chapter three presents evidence that loss of Q leads to poor bacterial replication and colonization inside the worm. l suggest that because Q-less E. coli diet have attenuated killing against C. elegans, Q should be considered a virulence factor.