ABSTRACT

Autophagy is a highly conserved homeostatic mechanism for the degradation and recycling of bulk cytoplasm, long-lived proteins, and cell organelles. It is triggered and modulated by a plethora of different stimuli such as nutrient deprivation and other stress signals. The process of autophagosome formation proceeds via initiation, elongation, and maturation steps leading to autophagic vesicles that, together with the cargo to be degraded, finally fuse with lysosomes to form the autophagolysosomes. The entire process of macroautophagy in particular the initial steps, are controlled by a large variety of autophagy related genes that are involved in the sequential formation of multimeric complexes. The chapter discusses the central role of glutamine in this regulatory network. Induction of autophagy has been associated with increased life span because it provides a quality-control mechanism that contributes to the turnover of aggregation-prone proteins and organelle homeostasis. The role of autophagy in tumorigenesis, tumor progression, and cancer therapeutics is indifferent and highly context dependent.