Long time-lapse imaging reveals unique features of PARK2/Parkin-mediated mitophagy in mature cortical neurons

Autophagy. 2012 Jun;8(6):976-8. doi: 10.4161/auto.20218. Epub 2012 Jun 1.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Cell Differentiation*
  • Cerebral Cortex / pathology*
  • Humans
  • Mice
  • Mitochondria / metabolism
  • Mitophagy*
  • Models, Biological
  • Neurons / metabolism*
  • Neurons / pathology*
  • Time-Lapse Imaging / methods*
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Ubiquitin-Protein Ligases
  • parkin protein