The LC3 recruitment mechanism is separate from Atg9L1-dependent membrane formation in the autophagic response againstSalmonella
Copyright policy )The LC3 recruitment mechanism is separate from Atg9L1-dependent membrane formation in the autophagic response againstSalmonella
Salmonella develops into resident bacteria in epithelial cells, and the autophagic machinery (Atg) is thought to play an important role in this process. In this paper, we show that an autophagosome-like double-membrane structure surrounds the Salmonella still residing within the Salmonella-containing vacuole (SCV). This double membrane is defective in Atg9L1- and FAK family-interacting protein of 200 kDa (FIP200)-deficient cells. Atg9L1 and FIP200 are important for autophagy-specific recruitment of the phosphatidylinositol 3-kinase (PI3K) complex. However, in the absence of Atg9L1, FIP200, and the PI3K complex, LC3 and its E3-like enzyme, the Atg16L complex, are still recruited to Salmonella. We propose that the LC3 system is recruited through a mechanism that is independent of isolation membrane generation.
- Osaka University Japan
- University of Michigan–Flint United States
- University of Michigan–Ann Arbor United States
Intracellular Signaling Peptides and Proteins, Vesicular Transport Proteins, Autophagy-Related Proteins, Membrane Proteins, Articles, Mice, Phosphatidylinositol 3-Kinases, Salmonella, Focal Adhesion Kinase 1, Phagosomes, Salmonella Infections, Vacuoles, Autophagy, NIH 3T3 Cells, Animals, Microtubule-Associated Proteins
Intracellular Signaling Peptides and Proteins, Vesicular Transport Proteins, Autophagy-Related Proteins, Membrane Proteins, Articles, Mice, Phosphatidylinositol 3-Kinases, Salmonella, Focal Adhesion Kinase 1, Phagosomes, Salmonella Infections, Vacuoles, Autophagy, NIH 3T3 Cells, Animals, Microtubule-Associated Proteins
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