Role of metabolic rate and DNA-repair in Drosophila aging: implications for the mitochondrial mutation theory of aging.

The respective roles of respiration rate and DNA repair in determining the life-span of Drosophila melanogaster have been investigated in three wild strains (Oregon R, Domodedov 32, & Swedish C) and two mutants (w/w & w/mei-41 D5). In agreement with the rate of living theory, there was an inverse relation between oxygen consumption and median life-span in flies having normal DNA repair. In contrast, w/mei-41 D5, showed an abnormally low life-span as compared to the controls. The median life-spans for these flies were: Oregon R, 49; Domodedov 32, 46; Swedish C, 35; w/w, 33; and w/mei-41 D5, 22. Furthermore, this mutant also showed significant deficiency in mating fitness and a depressed metabolic rate. These data suggest that the short life-span of the w/mei-41 D5 is a consequence of a specific syndrome unrelated to normal aging and is not the expression of accelerated senescence. It is proposed that DNA repair mechanisms influence adult life-span by their effect on actively dividing progenitor cells during development rather than by modulating senescence of the resulting differentiated cells of the imago during adulthood.