Investigations into Synergistic Effects of Longevity Mutations in Drosophila melanogaster

Mutations in many genes have been found that can increase the longevity of an organism. However, little work has been done on the interactions between these genes and how they cooperate to define the life span of the organism. To see if longevity mutation synergism could occur, I looked at the effect of combining multiple mutations known to significantly increase lifespan in Drosophila melanogaster. I placed methuselah (mth), Target of Rapamycin (Tor), ecdysone receptor (EcR), and rpd3 mutants in the w1118 wildtype background, and then crossed the mutants to obtain heterozygous double mutants. I carried out longevity assays on the progeny, and conducted statistical analyses to see if the mutants had synergistic (or other) effects on longevity. I observed that in the w1118 background, longevity mutants could indeed extend longevity, confirming previous results. I also found that, in a few cases, double mutants could have multiplicative increases in longevity relative to the single mutants. However, I could not find any examples of longevity mutant synergism. My results suggest that Tor and mth, and Rpd3 and mth, act through different pathways to extend longevity. They also imply that by combining multiple longevity-increasing interventions correspondingly increased longevity can be attained.