Autophagy L3

• Non-selective autophagy in response to starvation or in basal function, randomly removing material from the cellular cytosol at a constant level
• Selective autophagy uses cargo selection using LC3-ii and targets are recognised and tagged and included as ubiquinated proteins, dmged mitochondria and bacterial invaders
• p62 is an important adaptor protein, it gets consumed in degradation and gets regulated itself also invovled in infllammatory pathways.
• p62 has two domains an LIR domain which interacts with LC3-II on autophagosome and UBA-containing receptor protein that recongises ubiquitinaton.

  P62 aids the membrane via increasing curvature and accumulated LC3-II w/ or w/o lipid attachment. P62 binds polyubiq one side and LC3-II the other side and the membrane forms around forming a phaogphore, lysosome merges with autophagosome, makes autolysosome to degrade stuff.
• LC3-II has an attachment point for phosphotidy ethanamine, it interacts with the LIR domain of p62 and UBA interacts with the polyubiquitination of the degraded contents
• LIR motifi is important for autophagy because it enables binding to an adaptor protein LC3-II and binding to the aggregated proteins to be included in the autophagosome and interactions of adaptor proteins with LC3-II enable attachment to the microtuble network
• 1. During active stress the sec 62/63 complex translocates proteins LC3- II into ER to relocate them, signalling processes allow the ER to contract and extend a length and pulls off the ER to form the phagophore.
• There are lots of conformational changes that go on, spherical chape is induced via a conical lipid. Ubiquitination causes the complexes to cluster, scaffold and induce curvature.

  AMFR is a E3 ubiquitin ligase that LFAM 3AB ubiquitinates dimerises, complexes and forces a curvature to form