Gαq-mediated contact release is required for efficient mitochondrial quality control

Gq is required for efficient mitochondrial quality control by regulating mitochondria–lysosome contact dissociation at mitochondrial tips, and its loss causes prolonged tethering and altered mitophagy.

• Why it matters: Coordinated lysosome–mitochondria dynamics are essential for cellular homeostasis, yet how G protein signaling controls contact turnover and downstream mitochondrial quality control is unclear.
• What they did: The study identified Fis1 and RabGAPs TBC1D15/TBC1D17 as Gq partners using mitochondrial proteomics, co-immunoprecipitation, proximity ligation, and purified-protein binding, then tested Gq loss and rescue by re-expression.
• The result: Without Gq, lysosomes enlarge and cluster, mitochondria–lysosome contacts persist longer, and mitochondrial fission and mitophagic turnover shift; re-expressing Gq—but not an interaction-deficient mutant—restored normal contact dynamics, fragmentation, and mitophagy.

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