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How could Parkin-mediated ubiquitination of mitofusin promote mitophagy?
被引：48
作者：
Ziviani, Elena
Whitworth, Alexander J.
[1
]
机构：
[1] Univ Sheffield, MRC Ctr Dev & Biomed Genet, Sheffield, S Yorkshire, England
来源：
基金：
英国医学研究理事会;
英国惠康基金;
关键词：
Parkinson disease;
neurodegeneration;
Parkin;
PINK1;
Mfn;
mitochondrial dynamics;
ubiquitination;
Drosophila;
D O I：
10.4161/auto.6.5.12242
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ;
090102 ;
摘要：
Much evidence links mitochondrial dysfunction to the death of neurons in Parkinson disease (PD), and is particularly emphasized by our growing understanding of the function of genes linked to recessively inherited PD such as PINK1, parkin and DJ-1. Recent work has revealed an exciting link between the PINK1-Parkin pathway and the autophagic turnover of dysfunctional mitochondrial (mitophagy). We have recently shown that mitofusin is ubiquitinated by Parkin when it is recruited to dysfunctional mitochondria. Recent work also shows that regulated fission and fusion events help segregate dysfunctional mitochondria prior to mitophagy. Here we hypothesize how Parkin-mediated ubiquitination of Mfn may play a role in this mechanism.
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页码：660 / 662
页数：3
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