Mitochondria shed their outer membrane in response to infection-induced stress

Author:

Li Xianhe1ORCID,Straub Julian1ORCID,Medeiros Tânia Catarina1,Mehra Chahat1ORCID,den Brave Fabian2ORCID,Peker Esra3,Atanassov Ilian1ORCID,Stillger Katharina3ORCID,Michaelis Jonas Benjamin4,Burbridge Emma56,Adrain Colin56ORCID,Münch Christian4ORCID,Riemer Jan37ORCID,Becker Thomas2ORCID,Pernas Lena F.17ORCID

Affiliation:

1. Max Planck Institute for Biology of Ageing, Cologne, Germany.

2. Institute of Biochemistry and Molecular Biology, Medical Faculty, University of Bonn, Bonn, Germany.

3. Institute of Biochemistry, University of Cologne, Cologne, Germany.

4. Institute of Biochemistry II, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany.

5. Patrick G Johnston Centre for Cancer Research, Queen’s University Belfast, Belfast, Northern Ireland.

6. Instituto Gulbenkian de Ciência, Oeiras, Portugal.

7. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.

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

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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