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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.

Mev Dominquez-Valentin from the Department of Tumor Biology at the Institute for Cancer Research is senior author on a study recently published in the prestigious journal Clinical Gastroenterology and Hepatology, entitled: "Characterization of Screening Strategies for Lynch Syndrome in Latin America.” The study involves the collaborations of more than 50 investigators from 24 representative genetic cancer registries/center of 8 countries from Latin America, highlighting the significant insights we've gained into Lynch Syndrome (LS) screening methods across the region. The results emphasize challenges in hereditary cancer syndrome screening in Latin America and the need for enhanced strategies. Other OUS researchers involved in the study are Eivind Hovig, Pål Møller and Vessela Kristensen.