Autophagy ensures the lysosome-mediated breakdown and recycling of self-material,
as it not only degrades obsolete or damaged intracellular constituents but also provides
building blocks for biosynthetic and energy producing reactions. Studies in animal
models including Drosophila revealed that autophagy defects lead to the rapid decline
of neuromuscular function, neurodegeneration, sensitivity to stress (such as starvation
or oxidative damage), and stem cell loss. Of note, recently identified human Atg gene
mutations cause similar symptoms including ataxia and mental retardation. Physiologically,
autophagic degradation (flux) is known to decrease during aging, and this defect likely
contributes to the development of such age-associated diseases. Many manipulations
that extend lifespan (including dietary restriction, reduced TOR kinase signaling,
exercise or treatment with various anti-aging substances) require autophagy for their
beneficial effect on longevity, pointing to the key role of this housekeeping process.
Importantly, genetic (e.g., Atg8a overexpression in either neurons or muscle) or pharmacological
(e.g., feeding rapamycin or spermidine to animals) promotion of autophagy has been
successfully used to extend lifespan in Drosophila, suggesting that this intracellular
degradation pathway can rejuvenate cells and organisms. In this review, we highlight
key discoveries and recent progress in understanding the relationship of autophagy
and aging in Drosophila.
