Questions and Answers
What is the function of autophagy receptors in selective autophagy?
What is the region on autophagy receptors that interacts with LC3II?
Which of the following is a type of selective autophagy receptor?
What is the function of the ULK1 complex in autophagy?
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What is the result of LC3 lipidation?
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What is the function of ATG proteins in autophagy?
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What is the region on autophagy receptors that interacts with ubiquitin?
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Which of the following is NOT a type of selective autophagy receptor?
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What is a key characteristic of LC3-associated phagocytosis (LAP)?
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Which molecular complex is required for LC3-associated phagocytosis?
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Which of the following statements about LAP is true?
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What types of materials can be targeted through LC3-associated phagocytosis?
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What differentiates LAP from canonical autophagy?
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Which of the following components is dispensable for LC3-associated phagocytosis?
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Which process is NOT associated with LC3-associated phagocytosis?
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What activates the LAP pathway?
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What role do Atg8s play in autophagosome formation?
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Which ATG protein is recruited to membranes during the canonical autophagy process?
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What is the significance of LC3 lipidation in autophagy?
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Which protein complex involves recruitment during the initiation of autophagy?
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What is an alternative role of ATG16L1 in non-canonical pathways?
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What happens to mitochondria during the process described?
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Which membrane structure is represented in green in the 3D rendering?
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Which protein is NOT part of the ULK1 complex mentioned?
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Study Notes
LC3-associated Phagocytosis (LAP)
- LAP uses a portion of the canonical autophagy machinery
- Characterized by the conjugation of LC3 family proteins to phagosome membranes
- Cargos: pathogens, dying cells, soluble ligands, protein aggregates
- Involved in immune activation and inflammatory responses
LAP Pathway
- Not dependent on the AMPK–mTORC1–ULK1 axis
- Not responsive to nutrient status or intracellular stress sensing
- Activating stimulus from the cell exterior: ligands, pathogens, dying cells, immune complexes
- Requires the PI3KC3 complex composed of VPS34, VPS15, BECN1, ATG14L, UVRAG, RUBCN
- ULK complex (ULK1, FIP200, ATG13, ATG101) is dispensable for LAP
Autophagosome Formation and Expansion
- Atg8s are dispensable for autophagosome formation but regulate autophagosome expansion
- Hexa KO cell deficient for all ATG8/GABARAP members: 3D rendering of reconstructed autophagosomal compartment (green) and sequestered mitochondrion (red)
Non-Canonical Functions of ATG16L1
- Model for the recruitment of ATG16L1 to membranes:
- Induction of LC3 lipidation during autophagy depends on the ULK1 complex subunit FIP200 and WIPI2
- Recruitment of ATG16L1 to the site of autophagosome formation via the FBD, leading to LC3 conjugation to the isolation membrane
- During autophagy-unrelated, non-canonical pathways involving LC3 lipidation, ATG16L1 is recruited via its C-terminal WD40 domain and promotes the lipidation of LC3 to single membranes
Autophagy Receptors
- Autophagy receptors: p62, NBR1 (neighbor of BRCA1 gene 1), etc.
- Functions of autophagy receptors and adaptors in selective autophagy
- Selective recruitment of phagophores to cargos through the interaction of autophagy receptors with LC3II
- Selective autophagy types and corresponding receptors
- Regulatory modifications reported for selective autophagy receptors
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Description
LAP is a process that uses autophagy machinery to engulf and remove pathogens, dying cells, and other cargos, playing a role in immune activation and inflammation. It is activated by external stimuli and does not respond to nutrient status or intracellular stress.
