Mitochondria shed their outer membrane in response to infection-induced stress
Xianhe Li, Julian Straub, Tania Medeiros, Chahat Mehra, Fabian den Brave, Esra Peker, Ilian Atanassov, Katharina Stillger, Jonas B. Michaelis, Emma Burbridge, Colin Adrain, Christian Münch, Jan Riemer, Thomas Becker, Lena Pernas
Abstract
Mitochondria shed their SPOTs Outer mitochondrial membrane (OMM) function is essential for cellular health. How mitochondria respond to naturally occurring OMM stress is unknown. Li et al . show that, upon infection with the human parasite Toxoplasma gondii , mitochondria shed large structures positive for OMM (SPOTs). SPOT formation required the parasite effector TgMAF1 and its interaction with the host mitochondrial receptor TOM70 and translocase SAM50. TOM70-dependent SPOT formation mediated a depletion of mitochondrial proteins and optimal parasite growth. SPOT-like structures also formed after OMM perturbations independently of infection. Thus, membrane remodeling is a feature of cellular responses to OMM stress that Toxoplasma hijacks during infection. —SMH