Publication in Journal of Cell Biology: SNX10 as a modulator of mitochondrial protein turnover and mitochondrial bioenergetics
Mitochondria are essential for cellular energy production and homeostasis, and their selective degradation through mitophagy is critical for maintaining cell function. However, the molecular mechanisms governing this process remain incompletely understood.
Now, Laura Trachsel-Moncho and co-workers in Anne Simonsen’s group identify the endosomal protein SNX10 as a modulator of piecemeal mitophagy, a process involving the selective degradation of mitochondrial components. They show that SNX10 localizes to early endosomes in normal conditions but associates with mitochondria-containing endosomal structures under hypoxia-mimicking stress. Loss of SNX10 leads to increased turnover of specific mitochondrial proteins, reduced mitochondrial respiration, and elevated reactive oxygen species (ROS) levels. Furthermore, zebrafish larvae lacking Snx10 exhibit reduced COX-IV levels and increased oxidative stress and cell death, demonstrating the physiological relevance of Snx10 in mitochondrial homeostasis.
These findings uncover an unexpected role for SNX10 in mitochondrial quality control and highlight its importance in cellular adaptation to metabolic stress.
Links
The J Cell Biol article:
SNX10 functions as a modulator of piecemeal mitophagy and mitochondrial bioenergetics
Laura Trachsel-Moncho, Chiara Veroni, Benan John Mathai, Ana Lapao, Sakshi Singh, Nagham Theres Asp, Sebastian W. Schultz, Serhiy Pankiv and Anne Simonsen
J. Cell Biol. 2025 Vol. 224 No. 5 e202404009 https://doi.org/10.1083/jcb.202404009
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