Actin cages isolate damaged mitochondria during mitophagy |
| |
Authors: | Antonina J. Kruppa |
| |
Affiliation: | Department of Clinical Biochemistry, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK |
| |
Abstract: | Mitochondrial homeostasis is maintained by removing dysfunctional, ubiquitinated mitochondria from the network via PRKN-dependent mitophagy. MYO6, a unique myosin that moves towards the minus ends of actin filaments, forms a complex with PRKN and is selectively recruited to damaged mitochondria by binding to ubiquitin. On the mitochondrial surface, this myosin motor initiates the assembly of F-actin cages, which serve as a quality control mechanism to isolate dysfunctional mitochondria thereby preventing their refusion with neighboring populations. MYO6 also plays a role in the later stages of the mitophagy pathway by tethering endosomes to actin filaments facilitating mitophagosome maturation and autophagosome-lysosome fusion. |
| |
Keywords: | Actin mitochondrial quality control mitophagy MYO6 myosin VI PRKN Parkin |
|
|