期刊
AUTOPHAGY
卷 8, 期 6, 页码 976-978出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.20218
关键词
mitochondria; Parkin; PARK2; lysosome; autophagosome; autophagy; depolarization; mitochondrial mobility; neuronal mitophagy; mitochondrial membrane potential; mitochondrial quality control
类别
资金
- Intramural NIH HHS Funding Source: Medline
- NIA NIH HHS [R00 AG033658] Funding Source: Medline
Proper degradation of aged and damaged mitochondria through mitophagy is essential to ensure mitochondrial integrity and function. Translocation of PARK2/Parkin onto damaged mitochondria induces mitophagy in many non-neuronal cell types. However, direct evidence showing PARK2-mediated mitophagy in mature neurons is controversial, leaving unanswered questions as to how, where, and by what time course PARK2-mediated mitophagy occurs in neurons following mitochondrial depolarization. We applied long time-lapse imaging in live mature cortical neurons to monitor the slow but dynamic and spatial PARK2 translocation onto damaged mitochondria and subsequent degradation through the autophagy-lysosomal pathway. In comparison with non-neuronal cells, our study reveals unique features of PARK2-mediated mitophagy in mature neurons, which will advance our understanding of pathogenesis of several major neurodegenerative diseases characterized by damaged mitochondria or a dysfunctional autophagy-lysosomal system.
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