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Updated: May 7, 2026
06:14
Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
Published on: November 14, 2025
Atypical mitochondrial fission upon bacterial infection
Fabrizia Stavru1, Amy E Palmer, Chunxin Wang
1Unité des Interactions Bactéries-Cellules, Institut Pasteur, 75015 Paris, France.
Summary
Listeria monocytogenes infection fragments mitochondria via listeriolysin O (LLO), independent of canonical fission proteins like Drp1 and Opa1. The endoplasmic reticulum mediates this unique fragmentation process.
Area of Science:
- Cell Biology
- Microbiology
- Molecular Biology
Background:
- Listeria monocytogenes infection is known to cause mitochondrial network fragmentation.
- This fragmentation is mediated by the secreted pore-forming toxin listeriolysin O (LLO).
Purpose of the Study:
- To investigate the factors involved in canonical mitochondrial fusion and fission during Listeria infection.
- To elucidate the mechanism of LLO-induced mitochondrial fragmentation.
Main Methods:
- Examined canonical fusion and fission machinery components.
- Assessed the role of dynamin-like protein 1 (Drp1) and optic atrophy protein 1 (Opa1) in LLO-induced fragmentation.
- Investigated the involvement of the endoplasmic reticulum (ER) in mitochondrial fragmentation.
Main Results:
- LLO-induced mitochondrial fragmentation occurs independently of the canonical Drp1 fission machinery.
- Drp1 oligomers are absent, Mff receptor is degraded, and fragmentation is efficient in Drp1-impaired cells.
- Fragmentation proceeds without Opa1 processing, suggesting a unique fission mechanism distinct from uncouplers or staurosporine.
- The ER marks fragmentation sites even without functional Drp1, indicating ER-mediated fission.
Conclusions:
- Listeria toxin LLO induces mitochondrial fragmentation through a novel mechanism independent of Drp1 and Opa1.
- The endoplasmic reticulum plays a crucial role in this ER-mediated mitochondrial fission.
- This ER-driven process represents a unique pathway for mitochondrial fragmentation induced by exogenous agents.
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