TOPICS 2019
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Yang-Chi-Chun and Hisao Masai (Genome Dynamics Project) published a paper entitled ”Cdc7 activates replication checkpoint by phosphorylating the Chk1 binding domain of Claspin in human cells.” in eLife
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Hikaru Tsuchiya (Laboratory of Protein Metabolism) published a paper entitled “Structural insights into ubiquitin recognition and Ufd1 interaction of Npl4” in Nature Communications.
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Miharu Nakanishi (Mental Health Promotion Project) published a paper entitled ”Midlife Psychological Well-Being and its Impact on Cognitive Functioning Later in Life: An Observational Study Using a Female British Cohort.” in Journal of Alzheimer’s Disease
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Dr. Masato Hosokawa (Dementia Research Project) was awarded the Encouragement Award (Best Basic Research) at the Japan Society for Dementia Research Annual Meeting in 2019.
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Tetsuya Hirabayashi (Laboratory of Biomembrane）published a paper entitled "SDR9C7 catalyzes critical dehydrogenation of acylceramides for skin barrier formation" in The Journal of Clinical Investigation
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Yukio Nishimura (Neural Prosthesis Project) published a paper entitled ”Bypassing stroke-damaged neural pathways via a neural interface induces targeted cortical adaptation” in Nature Communications.
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Takahiko Noro (Visual Research Project) published a paper on glaucoma-like degeneration of the visual system in aged marmosets in Scientific Reports.
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Dr. Fumika Koyano (Ubiquitin Project) published a paper on “Parkin‐mediated ubiquitylation redistributes MITOL/March5 from mitochondria to peroxisomes” in EMBO Reports.
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Keisuke Kamimura (Neural Network Project) published a paper entitled ”The HSPG Glypican Regulates Experience-Dependent Synaptic and Behavioral Plasticity by Modulating the Non-Canonical BMP Pathway” in Cell Reports
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Takahiro Sanada (Viral Infectious Diseases Project) published a paper on “Construction of complete Tupaia belangeri transcriptome database by whole-genome and comprehensive RNA sequencing” in Scientific Reports
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Yuki Nakayama (ALS Nursing Care Project) published a paper on “Body weight variation predicts disease progression after invasive ventilation in amyotrophic lateral sclerosis” in Scientific Reports
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Kazuhiko Namekata (Visual Research Project) published a paper on the role of DOCK8 during neurodegeneration in Journal of Biological Chemistry.
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Daisuke Yamane (Viral Infectious Diseases Project) published a paper on “Basal Expression of Interferon Regulatory Factor 1 Drives Intrinsic Hepatocyte Resistance to Multiple RNA Viruses” in Nature Microbiology
HOME ＞ Topics2019 ＞ 10 October 2019
10 October 2019
Dr. Fumika Koyano (Ubiquitin Project) published a paper on “Parkin‐mediated ubiquitylation redistributes MITOL/March5 from mitochondria to peroxisomes” in EMBO Reports.
Parkin‐mediated ubiquitylation redistributes MITOL/March5 from mitochondria to peroxisomes
Summary
We found that mitochondrial E3 ubiquitin ligase MITOL/March5 translocates from depolarized mitochondria to peroxisomes following mitophagy stimulation. Interestingly, ubiquitylation of MITOL at K268 by Parkin is required for p97/VCP‐dependent extraction from damaged mitochondria.
Finally, we revealed that (1) MITOL is ubiquitylated in a PINK1/Parkin‐dependent manner in response to mitochondrial depolarization, (2) ubiquitylated MITOL translocates from mitochondria to peroxisomes instead of undergoing degradation, (3) specific peroxins (Pex3 and Pex16) and p97/VCP are required for MITOL translocation to peroxisomes, and (4) MITOL may affect peroxisomal size and abundance.
- ＜Title of the paper＞
- Parkin‐mediated ubiquitylation redistributes MITOL/March5 from mitochondria to peroxisomes
- ＜Journal＞
- EMBO Reports
DOI: 10.15252/embr.201947728
https://www.embopress.org/doi/10.15252/embr.201947728
Details
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.
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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