Autophagy, translated from Greek means to ‘self eat’. It is a basic catabolic mechanism involving cell degradation of unwanted or dysfunctional cellular components through the lysosome. Autophagy has been speculated to alter lifespan in organisms. Autophagy is triggered in response to varied stress and physiological conditions like food deficit, hyperthermia, etc. At molecular level, an autophagy pathway exhibits extraordinary interrelations with factors manipulating aging. This experiment was intended by the authors to deduce how autophagy genes affect life span on Caenorhabditis elegans with other longevity pathways and mechanisms.
In this study, the authors used wild type C. elegans and mutant C. elegans by RNA interference to generate clones. They used different techniques of epistasis, life span analysis, electron microscopy, age pigment measurement, and behavioral assay and obtained results correlating to various life-enhancing cellular pathways.
Many results were gathered from the study, the most prominent being how autophagy and the IGF pathway share an interesting relationship. It is already known that IGF-1/Insulin signaling pathway promotes reproductive growth and survival. It was found in C. elegans that insulin/IGF-1 signaling pathway cause the nematodes to enter the ‘dauer larva’ stage because of lack of nutrition and other factors; and, resulted in altered tissue aging from mutations in the IGF pathway, as well. Another interesting concept of the IGF pathway concerning autophagy is that the TOR signaling pathway interacts with IGF to regulate life span, and that the autophagy genes are required for this to lengthen the life span. Dietary restriction also regulates similar effects by destroying the long-term phenotype of distorted nematodes with mutations in the autophagy genes. It was also noted that autophagy genes are necessary for long life spans