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ATG16L1 meets ATG9 in recycling endosomes: additional roles for the plasma membrane and endocytosis in autophagosome biogenesis.

Puri C, Renna M, Bento CF, Moreau K, Rubinsztein DC - Autophagy (2013)

Bottom Line: Autophagosomes ultimately fuse with lysosomes, where their contents are degraded.The origin of the autophagosome membrane may involve different sources, such as mitochondria, Golgi, endoplasmic reticulum, plasma membrane, and recycling endosomes.We recently observed that ATG9 localizes on the plasma membrane in clathrin-coated structures and is internalized following a classical endocytic pathway through early and then recycling endosomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Genetics; Cambridge Institute for Medical Research; University of Cambridge; Cambridge UK.

ABSTRACT
Autophagosomes are formed by double-membraned structures, which engulf portions of cytoplasm. Autophagosomes ultimately fuse with lysosomes, where their contents are degraded. The origin of the autophagosome membrane may involve different sources, such as mitochondria, Golgi, endoplasmic reticulum, plasma membrane, and recycling endosomes. We recently observed that ATG9 localizes on the plasma membrane in clathrin-coated structures and is internalized following a classical endocytic pathway through early and then recycling endosomes. By contrast, ATG16L1 is also internalized by clathrin-mediated endocytosis but via different clathrin-coated pits, and appears to follow a different route to the recycling endosomes. The R-SNARE VAMP3 mediates the coalescence of the 2 different pools of vesicles (containing ATG16L1 or ATG9) in recycling endosomes. The heterotypic fusion between ATG16L1- and ATG9-containing vesicles strongly correlates with subsequent autophagosome formation. Thus, ATG9 and ATG16L1 both traffic from the plasma membrane to autophagic precursor structures and provide 2 routes from the plasma membrane to autophagosomes.

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Figure 1. Schematic diagram of ATG9 and ATG16L1 trafficking pathways, showing how they meet and fuse in a VAMP3-dependent manner in recycling endosomes.
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Figure 1: Figure 1. Schematic diagram of ATG9 and ATG16L1 trafficking pathways, showing how they meet and fuse in a VAMP3-dependent manner in recycling endosomes.

Mentions: We found that ATG9 trafficks through the plasma membrane and is internalized by clathrin-mediated endocytosis. After internalization, ATG9 is delivered to recycling endosomes via a conventional route through early endosomes, following the canonical transferrin receptor internalization pathway. Interestingly, the ATG16L1 and ATG9 are found in distinct clathrin-coated pits. Furthermore, these proteins appear to follow distinct paths to recycling endosomes, since there is no obvious localization of ATG16L1 in early endosomes (Fig. 1).


ATG16L1 meets ATG9 in recycling endosomes: additional roles for the plasma membrane and endocytosis in autophagosome biogenesis.

Puri C, Renna M, Bento CF, Moreau K, Rubinsztein DC - Autophagy (2013)

Figure 1. Schematic diagram of ATG9 and ATG16L1 trafficking pathways, showing how they meet and fuse in a VAMP3-dependent manner in recycling endosomes.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4389876&req=5

Figure 1: Figure 1. Schematic diagram of ATG9 and ATG16L1 trafficking pathways, showing how they meet and fuse in a VAMP3-dependent manner in recycling endosomes.
Mentions: We found that ATG9 trafficks through the plasma membrane and is internalized by clathrin-mediated endocytosis. After internalization, ATG9 is delivered to recycling endosomes via a conventional route through early endosomes, following the canonical transferrin receptor internalization pathway. Interestingly, the ATG16L1 and ATG9 are found in distinct clathrin-coated pits. Furthermore, these proteins appear to follow distinct paths to recycling endosomes, since there is no obvious localization of ATG16L1 in early endosomes (Fig. 1).

Bottom Line: Autophagosomes ultimately fuse with lysosomes, where their contents are degraded.The origin of the autophagosome membrane may involve different sources, such as mitochondria, Golgi, endoplasmic reticulum, plasma membrane, and recycling endosomes.We recently observed that ATG9 localizes on the plasma membrane in clathrin-coated structures and is internalized following a classical endocytic pathway through early and then recycling endosomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Genetics; Cambridge Institute for Medical Research; University of Cambridge; Cambridge UK.

ABSTRACT
Autophagosomes are formed by double-membraned structures, which engulf portions of cytoplasm. Autophagosomes ultimately fuse with lysosomes, where their contents are degraded. The origin of the autophagosome membrane may involve different sources, such as mitochondria, Golgi, endoplasmic reticulum, plasma membrane, and recycling endosomes. We recently observed that ATG9 localizes on the plasma membrane in clathrin-coated structures and is internalized following a classical endocytic pathway through early and then recycling endosomes. By contrast, ATG16L1 is also internalized by clathrin-mediated endocytosis but via different clathrin-coated pits, and appears to follow a different route to the recycling endosomes. The R-SNARE VAMP3 mediates the coalescence of the 2 different pools of vesicles (containing ATG16L1 or ATG9) in recycling endosomes. The heterotypic fusion between ATG16L1- and ATG9-containing vesicles strongly correlates with subsequent autophagosome formation. Thus, ATG9 and ATG16L1 both traffic from the plasma membrane to autophagic precursor structures and provide 2 routes from the plasma membrane to autophagosomes.

Show MeSH
Related in: MedlinePlus