Autophagy

How Autophagy Works
When it comes to managing stress, our cells function like efficient machines, quickly assessing the situation and finding ways to adjust. Autophagy—literally, “eating oneself”—is one way that cells deal with typical day-to-day stress (misfolded proteins, aged or defective organelles) as well as unexpected disasters (hypoxic conditions, serum starvation, viral infections). The cellular machinery either digests the damaged or defective molecules, effectively eliminating the stressors that threaten cell health, or, in the case of hypoxia and serum starvation, devours existing proteins and organelles to generate key nutrients for survival.

Much about the autophagic process is still not well understood, including its role in diseases such as cancer and neurodegeneration. Here we describe new fluorescence-based imaging tools to help visualize this important intracellular process.

(click to enlarge) Schematic depiction of the multistep autophagy pathway.

The Process The process of autophagy begins with the formation and elongation of isolation membranes, or phagophores. The cytoplasmic cargo is then sequestered, and the double-membrane autophagosome fuses with a lysosome to generate the autolysosome. Finally, degradation is achieved through the action of hydrolytic enzymes within the autolysosome. The Continual Study of Autophagy Autophagy was first described in 1963; however, only in the past decade has this pathway become the subject of intense study. Researchers have sought to gain further insight into the role basal autophagy plays in cell homeostasis and development, and to further elucidate the role of induced autophagy in the cell’s response to stress, microbial infection, and disease processes such as neurodegeneration, cancer, and others.