Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Receptor
The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identi...
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| Vydané v: | Cell Ročník 168; číslo 1-2; s. 224 - 238.e10 |
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| Hlavní autori: | , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
12.01.2017
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| Predmet: | |
| ISSN: | 1097-4172 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| Abstract | The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identify the inner mitochondrial membrane protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria for autophagic degradation. PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans. Our findings pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 that may underlie its roles in physiology, aging, and disease. |
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| AbstractList | The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identify the inner mitochondrial membrane protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria for autophagic degradation. PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans. Our findings pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 that may underlie its roles in physiology, aging, and disease. The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identify the inner mitochondrial membrane protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria for autophagic degradation. PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans. Our findings pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 that may underlie its roles in physiology, aging, and disease. |
| Author | Chiang, Wei-Chung Wei, Yongjie Mishra, Prashant Sumpter, Jr, Rhea Levine, Beth |
| Author_xml | – sequence: 1 givenname: Yongjie surname: Wei fullname: Wei, Yongjie organization: Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA – sequence: 2 givenname: Wei-Chung surname: Chiang fullname: Chiang, Wei-Chung organization: Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA – sequence: 3 givenname: Rhea surname: Sumpter, Jr fullname: Sumpter, Jr, Rhea organization: Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA – sequence: 4 givenname: Prashant surname: Mishra fullname: Mishra, Prashant organization: Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA – sequence: 5 givenname: Beth surname: Levine fullname: Levine, Beth email: beth.levine@utsouthwestern.edu organization: Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA. Electronic address: beth.levine@utsouthwestern.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28017329$$D View this record in MEDLINE/PubMed |
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| Title | Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Receptor |
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