Related Experiment Video
Updated: Oct 6, 2025

Author Spotlight: Decoding Mitochondrial Aging
Published on: June 30, 2023
Mitochondria shed their outer membrane in response to infection-induced stress
Xianhe Li1, Julian Straub1, Tânia Catarina Medeiros1
1Max Planck Institute for Biology of Ageing, Cologne, Germany.
Abstract:
The outer mitochondrial membrane (OMM) is essential for cellular homeostasis. Yet little is known of the mechanisms that remodel it during natural stresses. We found that large “SPOTs” (structures positive for OMM) emerge during Toxoplasma gondii infection in mammalian cells. SPOTs mediated the depletion of the OMM proteins mitofusin 1 and 2, which restrict parasite growth. The formation of SPOTs depended on the parasite effector TgMAF1 and the host mitochondrial import receptor TOM70, which is required for optimal parasite proliferation. TOM70 enabled TgMAF1 to interact with the host OMM translocase SAM50. The ablation of SAM50 or the overexpression of an OMM-targeted protein promoted OMM remodeling independently of infection. Thus, Toxoplasma hijacks the formation of SPOTs, a cellular response to OMM stress, to promote its growth.
Insights
Toxoplasma gondii infection triggers the formation of large structures called SPOTs on the outer mitochondrial membrane (OMM). This process depletes OMM proteins, promoting parasite growth.
Area of Science:
- Cell Biology
- Parasitology
- Mitochondrial Biology
Background:
- The outer mitochondrial membrane (OMM) is crucial for cellular function.
- Mechanisms of OMM remodeling during cellular stress are not well understood.
- Toxoplasma gondii infection impacts host cell homeostasis.
Purpose of the Study:
- To investigate the remodeling of the OMM during Toxoplasma gondii infection.
- To identify host and parasite factors involved in OMM changes.
- To understand how these OMM changes affect parasite proliferation.
Main Methods:
- Observation of "SPOTs" (structures positive for OMM) in infected mammalian cells.
- Analysis of OMM protein depletion (mitofusin 1 and 2).
- Investigating the roles of parasite effector TgMAF1 and host receptor TOM70.
Main Results:
- Large SPOTs form on the OMM during T. gondii infection.
- SPOTs lead to the depletion of mitofusin 1 and 2, hindering parasite growth restriction.
- Parasite effector TgMAF1 and host receptor TOM70 are essential for SPOT formation.
- TOM70 facilitates TgMAF1 interaction with SAM50, an OMM translocase.
Conclusions:
- Toxoplasma gondii hijacks the host's OMM stress response pathway (SPOT formation) to promote its own growth.
- The parasite manipulates OMM protein levels via TgMAF1, TOM70, and SAM50.
- OMM remodeling can be induced independently of infection, highlighting its role in cellular stress responses.
Related Concept Videos
Mitochondrial Membranes
The Inner Mitochondrial Membrane
Porin Insertion in the Outer Mitochondrial Membrane
Three models describe the assembly of porins by the SAM complex and their insertion into the outer membrane. Model 1 suggests that porins are assembled outside the SAM channel as the...
Autophagy
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Translocation of Proteins into the Mitochondria
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Mitochondria

