SNX10 at the crossroad of endocytosis and piecemeal mitophagy

Mitophagy targets damaged or dysfunctional mitochondria for lysosomal degradation. While canonical mitophagy pathways target the whole mitochondria for lysosomal degradation, it has become clear that selected mitochondrial components can be targeted for lysosomal degradation via other pathways, such as piecemeal mitophagy or mitochondria-derived vesicles. In a recent study, we identified the PX domain-containing endosomal protein SNX10 as a negative modulator of piecemeal mitophagy. Endosomal SNX10-positive vesicles dynamically interact with mitochondria and acquire selected mitochondrial proteins upon hypoxia. Zebrafish larvae lacking Snx10 show elevated Cox-IV degradation, increased levels of reactive oxygen species (ROS), and ROS-dependent neuronal death.

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Publication Details

Journal
Autophagy
Published
2025-05-06
DOI
https://doi.org/10.1080/15548627.2025.2499641
Primary Topic
RNA Research and Splicing
Type
article
Field-Weighted Citation Impact
0.00

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article

SNX10 at the crossroad of endocytosis and piecemeal mitophagy

Benan John Mathai, Anne Simonsen, Laura Trachsel-Moncho, Chiara Veroni
1 links
Autophagy
RNA Research and Splicing
article

SNX10 at the crossroad of endocytosis and piecemeal mitophagy

Benan John Mathai, Anne Simonsen, Laura Trachsel-Moncho, Chiara Veroni
article en

Abstract

Mitophagy targets damaged or dysfunctional mitochondria for lysosomal degradation. While canonical mitophagy pathways target the whole mitochondria for lysosomal degradation, it has become clear that selected mitochondrial components can be targeted for lysosomal degradation via other pathways, such as piecemeal mitophagy or mitochondria-derived vesicles. In a recent study, we identified the PX domain-containing endosomal protein SNX10 as a negative modulator of piecemeal mitophagy. Endosomal SNX10-positive vesicles dynamically interact with mitochondria and acquire selected mitochondrial proteins upon hypoxia. Zebrafish larvae lacking Snx10 show elevated Cox-IV degradation, increased levels of reactive oxygen species (ROS), and ROS-dependent neuronal death.

AutophagyVol. 21(9)
Oslo University Hospital (NO), University of Oslo (NO)
Kreftforeningen, Helse Sør-Øst RHF
Zero hunger
Openalex Percentile: Top 91%
RNA Research and Splicing
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