Cytoplasmic genomes that confer additionallongevity in Drosophila melanogaster

Abstract

The mitochondrial genome has been proposed as aprincipal site of somatic mutation during ageing. Avariation of the error catastrophe model has beenproposed, in which ROS damages the mitochondrialgenome, which leads to additional ROS production in apositive feed back cycle. This leads to major DNAdamage, bioenergy crisis, and reduced functionalcapacity in old age and contributes to mortality.Therefore it might be expected that in strains inwhich the mitochondrial genomes vary, ROS andbioenergy crisis should covary and negativelycorrelate with longevity.Strains of Drosophila were produced whichdiffered in their mitochondria by breeding maternallyinherited genomes onto a common nuclear background. Thedonor strains included two long lived and two controlstrains. Those strains that had the cytoplasmicgenomes from the long-lived strains were also longlived. In these strains ROS production in young fliesnegatively correlated with longevity supporting a rolefor ROS in ageing and/or the death process.Ageing Drosophila show a failure in bioenergy, but therelative strength of this phenotype does not segregatewith longevity. These data do not support the errorcatastrophe model, but suggests that the principaloutcome of ROS damage that leads to death is notbioenergy failure, and that bioenergy failure is atleast partly due to non-ROS processes.