Actin cages isolate damaged mitochondria during mitophagy.
Accepted version
Peer-reviewed
Repository URI
Repository DOI
Change log
Authors
Kruppa, Antonina J
Buss, Folma https://orcid.org/0000-0003-4457-3479
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.
Description
Keywords
Actin, MYO6, PRKN, Parkin, mitochondrial quality control, mitophagy, myosin VI, Actins, Autophagy, HeLa Cells, Humans, Mitochondria, Mitophagy, Myosin Heavy Chains, Ubiquitin-Protein Ligases
Journal Title
Autophagy
Conference Name
Journal ISSN
1554-8627
1554-8635
1554-8635
Volume Title
14
Publisher
Informa UK Limited
Publisher DOI
Sponsorship
British Heart Foundation (PG/15/12/31280)
Medical Research Council (MR/N000048/1)
Medical Research Council (MR/K000888/1)
Michael J Fox Foundation (MJFF) (15669)
Medical Research Council (MR/N000048/1)
Medical Research Council (MR/K000888/1)
Michael J Fox Foundation (MJFF) (15669)