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NIPSNAP1 and NIPSNAP2 act as "eat me" signals to allow sustained recruitment of autophagy receptors during mitophagy.
- Source :
-
Autophagy [Autophagy] 2019 Oct; Vol. 15 (10), pp. 1845-1847. Date of Electronic Publication: 2019 Jul 04. - Publication Year :
- 2019
-
Abstract
- Removal of damaged mitochondria is vital for cellular homeostasis especially in non-dividing cells, like neurons. Damaged mitochondria that cannot be repaired by the ubiquitin-proteasomal system are cleared by a form of selective autophagy known as mitophagy. Following damage, mitochondria become labelled with 'eat-me' signals that selectively determine their degradation. Recently, we identified the mitochondrial matrix proteins, NIPSNAP1 (nipsnap homolog 1) and NIPSNAP2 as 'eat-me' signals for damaged mitochondria. NIPSNAP1 and NIPSNAP2 accumulate on the mitochondrial outer membrane following mitochondrial depolarization, recruiting autophagy receptors and adaptors, as well as human Atg8 (autophagy-related 8)-family proteins to facilitate mitophagy. The NIPSNAPs allow a sustained recruitment of SQSTM1-like receptors (SLRs) to ensure efficient mitophagy. Zebrafish lacking Nipsnap1 show decreased mitophagy in the brain coupled with increased ROS production, loss of dopaminergic neurons and strongly reduced locomotion.
- Subjects :
- Animals
Animals, Genetically Modified
Autophagy
Autophagy-Related Protein 8 Family genetics
Autophagy-Related Protein 8 Family metabolism
Gene Knockout Techniques
HeLa Cells
Humans
Protein Binding
Sequestosome-1 Protein chemistry
Sequestosome-1 Protein metabolism
Signal Transduction genetics
Zebrafish
Autophagy-Related Proteins metabolism
Intercellular Signaling Peptides and Proteins physiology
Intracellular Signaling Peptides and Proteins physiology
Membrane Proteins physiology
Mitophagy genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1554-8635
- Volume :
- 15
- Issue :
- 10
- Database :
- MEDLINE
- Journal :
- Autophagy
- Publication Type :
- Academic Journal
- Accession number :
- 31251109
- Full Text :
- https://doi.org/10.1080/15548627.2019.1637642