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NDP52 acts as a redox sensor in PINK1/Parkin-mediated mitophagy

The EMBO Journal (2022) e111372
PMID: 10.15252/embj.2022111372
The EMBO Journal (2022) e111372
PMID: 10.15252/embj.2022111372

Mitophagy, the elimination of mitochondria via the autophagy-lysosome pathway, is essential for the maintenance of cellular homeostasis. The best characterised mitophagy pathway is mediated by stabilisation of the protein kinase PINK1 and recruitment of the ubiquitin ligase Parkin to damaged mitochondria. Ubiquitinated mitochondrial surface proteins are recognised by autophagy receptors including NDP52 which initiate the formation of an autophagic vesicle around the mitochondria. Damaged mitochondria also generate reactive oxygen species (ROS) which have been proposed to act as a signal for mitophagy, however the mechanism of ROS sensing is unknown. Here we found that oxidation of NDP52 is essential for the efficient PINK1/Parkin-dependent mitophagy. We identified redox-sensitive cysteine residues involved in disulphide bond formation and oligomerisation of NDP52 on damaged mitochondria. Oligomerisation of NDP52 facilitates the recruitment of autophagy machinery for rapid mitochondrial degradation. We propose that redox sensing by NDP52 allows mitophagy to function as a mechanism of oxidative

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J Biol Chem 297(2) 100919

D. Pokorny, L. Truebestein, K. D. Fleming, J. E. Burke, and T. A. Leonard

J Biol Chem 297(2) 100919
D. Pokorny, L. Truebestein, K. D. Fleming, J. E. Burke, and T. A. Leonard
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Cooperative genetic networks drive embryonic stem cell transition from naïve to formative pluripotency

EMBO J 40:e105776

A. Lackner, R. Sehlke, M. Garmhausen, G. G. Stirparo, M. Huth, F. Titz-Teixeira, P. van der Lelij, J. Ramesmayer, H. F. Thomas, M. Ralser, L. Santini, E. Galimberti, M. Sarov, A. F. Stewart, A. Smith, A. Beyer, and M. Leeb

EMBO J 40:e105776
A. Lackner, R. Sehlke, M. Garmhausen, G. G. Stirparo, M. Huth, F. Titz-Teixeira, P. van der Lelij, J. Ramesmayer, H. F. Thomas, M. Ralser, L. Santini, E. Galimberti, M. Sarov, A. F. Stewart, A. Smith, A. Beyer, and M. Leeb
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