FIP200 regulates targeting of Atg16L1 to the isolation membrane |
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| Authors: | Taki Nishimura Takeshi Kaizuka Ken Cadwell Mayurbhai H Sahani Tatsuya Saitoh Shizuo Akira Herbert W Virgin Noboru Mizushima |
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| Institution: | 1. Department of Physiology and Cell Biology, Tokyo Medical and Dental University, , Tokyo, 113‐8519;2. Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, , Tokyo, 113‐0033 Japan;3. Department of Pathology and Immunology, Washington University School of Medicine, , Saint Louis, Missouri, 63110;4. Skirball Institute and Department of Microbiology, New York University School of Medicine, , New York, New York, 10016 USA;5. Laboratory of Host Defense, WPI Immunology Frontier Research Center;6. Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, , Suita, Osaka, 565‐0871 Japan |
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| Abstract: | Autophagosome formation is a dynamic process that is strictly controlled by autophagy‐related (Atg) proteins. However, how these Atg proteins are recruited to the autophagosome formation site or autophagic membranes remains poorly understood. Here, we found that FIP200, which is involved in proximal events, directly interacts with Atg16L1, one of the downstream Atg factors, in an Atg14‐ and phosphatidylinositol 3‐kinase‐independent manner. Atg16L1 deletion mutants, which lack the FIP200‐interacting domain, are defective in proper membrane targeting. Thus, FIP200 regulates not only early events but also late events of autophagosome formation through direct interaction with Atg16L1. |
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| Keywords: | autophagy FIP200 ULK1 Atg16L1 |
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