Parkin suppresses Drp1-independent mitochondrial division.

摘要: The cycle of mitochondrial division and fusion disconnect reconnect individual mitochondria in cells to remodel this energy-producing organelle. Although dynamin-related protein 1 (Drp1) plays a major role cells, reduced level still persists even the absence Drp1. It is unknown how much Drp1-mediated accounts for connectivity mitochondria. Parkinson's disease-associated protein-parkin, which biochemically genetically interacts with Drp1-in also remains poorly understood. Here, we quantified number using mitochondria-targeted photoactivatable GFP cells. We show that loss Drp1 increases by 15-fold mouse embryonic fibroblasts (MEFs). While single parkin does not affect mitochondria, significantly decreased compared when was lost Furthermore, frequency depolarization inner membrane caused increased Drp1-knockout MEFs. Therefore, our data suggest negatively regulates Drp1-indendent division.