Repository logo
 

Actin cages isolate damaged mitochondria during mitophagy.

Accepted version
Peer-reviewed

No Thumbnail Available

Type

Article

Change log

Authors

Kruppa, Antonina J 

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

Volume Title

14

Publisher

Informa UK Limited
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)