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Mitochondria play a critical role in aging, however, the underlying mechanism is not well understood. We found that a mutation disrupting the  C .  elegans  homolog of Miro GTPase ( miro-1 ) extends life span. This phenotype requires simultaneous loss of  miro-1  from multiple tissues including muscles and neurons, and is dependent on  daf-16/FOXO . Notably, the amount of mitochondria in the  miro-1  mutant is reduced to approximately 50% of the wild-type. Despite this reduction, oxygen consumption is only weakly reduced, suggesting that mitochondria of  miro-1  mutants are more active than wild-type mitochondria. The ROS damage is slightly reduced and the mitochondrial unfolded protein response pathway is weakly activated in  miro-1  mutants. Unlike previously described long-lived mitochondrial electron transport chain mutants,  miro-1  mutants have normal growth rate. These results suggest that the reduction in the amount of mitochondria can affect the life span of an organism through activation of stress pathways.

C. elegans miro-1 Mutation Reduces the Amount of Mitochondria and Extends Life Span