PUBLICATION

NIPSNAP1 and NIPSNAP2 Act as "Eat Me" Signals for Mitophagy

Authors
Princely Abudu, Y., Pankiv, S., Mathai, B.J., Håkon Lystad, A., Bindesbøll, C., Brenne, H.B., Yoke Wui Ng, M., Thiede, B., Yamamoto, A., Mutugi Nthiga, T., Lamark, T., Esguerra, C.V., Johansen, T., Simonsen, A.
ID
ZDB-PUB-190416-9
Date
2019
Source
Developmental Cell   49(4): 509-525.e12 (Journal)
Registered Authors
Esguerra, Camila V., Johansen, Terje
Keywords
ALFY, NDP52, NIPSNAP1, NIPSNAP2, Parkin, TAX1BP1, autophagy, mitophagy, optineurin, p62/SQSTM1
MeSH Terms
  • Adaptor Proteins, Signal Transducing/metabolism
  • Animals
  • Autophagy/physiology
  • Autophagy-Related Protein 8 Family/metabolism
  • Carrier Proteins/metabolism
  • HEK293 Cells
  • HeLa Cells
  • Humans
  • Intercellular Signaling Peptides and Proteins/metabolism*
  • Intracellular Signaling Peptides and Proteins/metabolism*
  • Membrane Proteins/metabolism*
  • Microtubule-Associated Proteins/metabolism
  • Mitochondria/metabolism
  • Mitochondrial Proteins/metabolism
  • Mitophagy/physiology*
  • Neurons/metabolism
  • Protein Binding
  • RNA-Binding Proteins/metabolism
  • Sequestosome-1 Protein/metabolism
  • Transcription Factors/metabolism
  • Ubiquitin-Protein Ligases/metabolism
  • Zebrafish
  • Zebrafish Proteins/metabolism*
PubMed
30982665 Full text @ Dev. Cell
Abstract
The clearance of damaged or dysfunctional mitochondria by selective autophagy (mitophagy) is important for cellular homeostasis and prevention of disease. Our understanding of the mitochondrial signals that trigger their recognition and targeting by mitophagy is limited. Here, we show that the mitochondrial matrix proteins 4-Nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1) and NIPSNAP2 accumulate on the mitochondria surface upon mitochondrial depolarization. There, they recruit proteins involved in selective autophagy, including autophagy receptors and ATG8 proteins, thereby functioning as an "eat me" signal for mitophagy. NIPSNAP1 and NIPSNAP2 have a redundant function in mitophagy and are predominantly expressed in different tissues. Zebrafish lacking a functional Nipsnap1 display reduced mitophagy in the brain and parkinsonian phenotypes, including loss of tyrosine hydroxylase (Th1)-positive dopaminergic (DA) neurons, reduced motor activity, and increased oxidative stress.
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