In eukaryotes, mitochondria house the electron transport apparatus essential for the efficient production of ATP, and as a consequence they are also the primary source of damaging reactive oxygen species (ROS). The mitochondrial genome of C. elegans is approximately 13.8 kbp and encodes 2 rRNAs, 22 tRNAs, and 12 proteins that work in unison with nuclear encoded proteins to compose the mitochondrial respiratory chain (MRC). Here, I am studying the 3 kbp uaDf5 mtDNA deletion which removes parts or all of 7 tRNA genes and 4 MRC protein genes. Worms are heteroplasmic for the deletion, bearing both deleted and full-length chromosomes, so the ratio of the deleted genes, (ND1, ATP6, ND2, and Cytb) is altered. We report that these heteroplasmic worms are metabolically challenged. They live significantly shorter lives, and lifespan is negatively correlated with the proportion of the deleted chromosome. I have found a significantly higher production of ROS in heteroplasmic worms. I propose that the increase of ROS is responsible for the premature aging of the uaDf5 mutants. These metabolic problems are not overcome by treatment of Coenzyme Q10 or increased ATP associated with a mutation gene
ucp-4.