Severe mitochondria deficiency leads to a number of devastating degenerative 
disorders, yet, mild mitochondrial dysfunction in different species, including 
the nematode Caenorhabditis elegans, can have pro-longevity effects. This 
apparent paradox indicates that cellular adaptation to partial mitochondrial 
stress can induce beneficial responses, but how this is achieved is largely 
unknown. Complete absence of frataxin, the mitochondrial protein defective in 
patients with Friedreich's ataxia, is lethal in C. elegans, while its partial 
deficiency extends animal lifespan in a p53 dependent manner. In this paper we 
provide further insight into frataxin control of C. elegans longevity by showing 
that a substantial reduction of frataxin protein expression is required to 
extend lifespan, affect sensory neurons functionality, remodel lipid metabolism 
and trigger autophagy. We find that Beclin and p53 genes are required to induce 
autophagy and concurrently reduce lipid storages and extend animal lifespan in 
response to frataxin suppression. Reciprocally, frataxin expression modulates 
autophagy in the absence of p53. Human Friedreich ataxia-derived lymphoblasts 
also display increased autophagy, indicating an evolutionarily conserved 
response to reduced frataxin expression. In sum, we demonstrate a causal 
connection between induction of autophagy and lifespan extension following 
reduced frataxin expression, thus providing the rationale for investigating 
autophagy in the pathogenesis and treatment of Friedreich's ataxia and possibly 
other human mitochondria-associated disorders.