Journal
DEVELOPMENTAL CELL
Volume 44, Issue 4, Pages 484-+Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2018.01.007
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Funding
- Wellcome Trust [100140, 093026, 102770/Z/13/Z]
- Medical Research Council [MR/K000888/1, MR/N000048/1, U105184323, U105697135, RG89175/SMAG/005]
- British Heart Foundation [PG/15/12/31280]
- Biotechnology and Biological Sciences Research Council [BB/K001981/1]
- Michael J. Fox Foundation
- BBSRC [BB/K001981/1] Funding Source: UKRI
- MRC [MR/K000888/1, MC_U105697135, MR/N000048/1, MC_UP_A025_1013, MC_UU_00015/4] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K001981/1] Funding Source: researchfish
- British Heart Foundation [PG/15/12/31280] Funding Source: researchfish
- Medical Research Council [MR/N000048/1, MR/K000888/1, MC_UU_00015/4, MC_U105697135] Funding Source: researchfish
- Wellcome Trust [102770/Z/13/Z] Funding Source: researchfish
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Mitochondrial quality control is essential to maintain cellular homeostasis and is achieved by removing damaged, ubiquitinated mitochondria via Parkinmediated mitophagy. Here, we demonstrate that MYO6 (myosin VI), a unique myosin that moves toward the minus end of actin filaments, forms a complex with Parkin and is selectively recruited to damaged mitochondria via its ubiquitin-binding domain. This myosin motor initiates the assembly of F-actin cages to encapsulate damaged mitochondria by forming a physical barrier that prevents refusion with neighboring populations. Loss of MYO6 results in an accumulation of mitophagosomes and an increase in mitochondrial mass. In addition, we observe downstream mitochondrial dysfunction manifesting as reduced respiratory capacity and decreased ability to rely on oxidative phosphorylation for energy production. Our work uncovers a crucial step in mitochondrial quality control: the formation of MYO6-dependent actin cages that ensure isolation of damaged mitochondria from the network.
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