PARK2/Parkin becomes critical when DNM1L/Drp1 is absent

Autophagy. 2015;11(3):573-4. doi: 10.1080/15548627.2015.1017193.


Maintaining mitochondrial dynamics and proper execution of mitophagy is crucial for sustaining cellular health. Defects in these processes have been linked to cardiovascular diseases and neurodegeneration. In a recent publication, we reported that the mitochondrial division dynamin protein DNM1L/Drp1 and the E3 ubiquitin ligase PARK2/Parkin work in a synergistic manner to maintain mitochondrial function and structural integrity in the mouse heart and brain.

Keywords: Drp1; Parkin; mitochondrial dynamics; mitochondrial homeostasis; mitophagy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / metabolism
  • Disease Models, Animal
  • Dynamins / metabolism*
  • Fibroblasts / metabolism
  • Gene Expression Regulation
  • Mice
  • Mice, Knockout
  • Mitochondria / metabolism*
  • Mitochondrial Dynamics
  • Mitochondrial Proteins / metabolism
  • Mitophagy*
  • Myocardium / metabolism
  • Neurons / metabolism
  • Parkinson Disease / genetics
  • Ubiquitin-Protein Ligases / metabolism*


  • Mitochondrial Proteins
  • Ubiquitin-Protein Ligases
  • parkin protein
  • Dnm1l protein, mouse
  • Dynamins