Macroautophagy Essay

Macroautophagy, a cellular process regulated by p53 is an intracellular system that involves the break down of cytoplasmic contents within the lysosome. This mechanism is a form of adaptation to cellular stress such as starvation, trophic factor deprivation, hypoxia, endoplasmic reticulum (ER) stress and oxidative stress (Levine & Abrams, 2008). Through adaptation, it allows the prevention of cell death. There are three types of autophagy: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). They all are involved in the degradation of cytosolic constituents in the lysosome. Through selective and non-selective mechanisms, macroautophagy and microautophagy are able to fuse with large cellular structures whereas chaperone-mediated autophagy on the other hand, has targeted
It also serves a maintenance role in the selective mechanism of autophagy whereby damaged parts of cells are collected by the autophagosome (an organelle that mediates autophagy) and taken to the vacuole where they are destroyed or further broken down to be reused. Autophagy begins with phagophore formation, Atg5-Atg 12 conjugation, and interaction with Atg16L. Also LC3 processing follows with the capturing of the cell targets for degradation. Fusion of the autophagosome then follows along with the proteolytic degradation by the lysosomal proteases of engulfed molecules (Glick, et. al, 2010). In the regulation of induction process, mTOR Ser/Thr kinase is de-repressed thus inhibiting autophagy through the phosphorylation of autophagy-protein-13 (Atg13). Due to this phosphorylation, Atg 13 dissociates from the protein complex containing Atg 1 kinase and Atg 17 therefore attenuating the activity of the Atg 1 kinase. With mTor inhibited, the dephosphorylated Atg 13 re-associates Atg 1 thus inducing autophagy (