ID | 115092 |
Author |
Koyano, Fumika
Tokyo Metropolitan Institute of Medical Science
Yamano, Koji
Tokyo Metropolitan Institute of Medical Science
Kosako, Hidetaka
Tokushima University
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Kimura, Yoko
Shizuoka University
Kimura, Mayumi
Tokyo Metropolitan Institute of Medical Science
Fujiki, Yukio
Kyushu University
Tanaka, Keiji
Tokyo Metropolitan Institute of Medical Science
Matsuda, Noriyuki
Tokyo Metropolitan Institute of Medical Science
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Keywords | March5
peroxin
PINK1- and Parkin-mediated mitophagy
ubiquitin
VCP
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Content Type |
Journal Article
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Description | Ubiquitylation of outer mitochondrial membrane (OMM) proteins is closely related to the onset of familial Parkinson's disease. Typically, a reduction in the mitochondrial membrane potential results in Parkin‐mediated ubiquitylation of OMM proteins, which are then targeted for proteasomal and mitophagic degradation. The role of ubiquitylation of OMM proteins with non‐degradative fates, however, remains poorly understood. In this study, we find that the mitochondrial E3 ubiquitin ligase MITOL/March5 translocates from depolarized mitochondria to peroxisomes following mitophagy stimulation. This unusual redistribution is mediated by peroxins (peroxisomal biogenesis factors) Pex3/16 and requires the E3 ligase activity of Parkin, which ubiquitylates K268 in the MITOL C‐terminus, essential for p97/VCP‐dependent mitochondrial extraction of MITOL. These findings imply that ubiquitylation directs peroxisomal translocation of MITOL upon mitophagy stimulation and reveal a novel role for ubiquitin as a sorting signal that allows certain specialized proteins to escape from damaged mitochondria.
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Journal Title |
EMBO Reports
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ISSN | 14693178
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Publisher | EMBO Press
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Volume | 20
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Issue | 12
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Start Page | e47728
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Published Date | 2019-10-10
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Rights | This is an open access article under the terms of the Creative Commons Attribution 4.0 License(https://creativecommons.org/licenses/by/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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DOI (Published Version) | |
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language |
eng
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TextVersion |
Publisher
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departments |
Institute of Advanced Medical Sciences
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