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Updated: Aug 17, 2026

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
Published on: November 14, 2025
The mitochondrial protein MTP18 contributes to mitochondrial fission in mammalian cells
Daniel Tondera1, Frank Czauderna, Katharina Paulick
1Atugen AG, Robert-Rössle-Strasse 10, Otto-Warburg-Haus (80), 13125 Berlin, Germany.
Abstract:
Mitochondria are dynamic organelles that change morphology by controlled fission and fusion events. Mitochondrial fission is regulated by a conserved protein complex assembled at the outer membrane. Human MTP18 is a novel nuclear-encoded mitochondrial membrane protein, implicated in controlling mitochondrial fission. Upon overexpression of MTP18, mitochondrial morphology was altered from filamentous to punctate structures suggesting excessive mitochondrial fission. Mitochondrial fragmentation was blocked in cells coexpressing either the mitochondrial fusion protein Mfn1 or Drp1(K38A), a dominant negative version of the fission protein Drp1. Also, a loss-of function of endogenous MTP18 by RNA interference (RNAi) resulted in highly fused mitochondria. Moreover, MTP18 appears to be required for mitochondrial fission because it is blocked after overexpression of hFis1 in cells with RNAi-mediated MTP18 knockdown. In conclusion, we propose that MTP18 functions as an essential intramitochondrial component of the mitochondrial division apparatus, contributing to the maintenance of mitochondrial morphology.
Insights
Mitochondrial fission protein MTP18 controls organelle shape. Overexpression causes fragmentation, while its loss leads to fused mitochondria, highlighting MTP18
Area of Science:
- Cell Biology
- Mitochondrial Dynamics
- Molecular Genetics
Background:
- Mitochondria are dynamic organelles undergoing continuous fission and fusion to maintain cellular function.
- Mitochondrial fission, a key process for organelle morphology, is regulated by a protein complex at the outer membrane.
Purpose of the Study:
- To investigate the role of the novel human mitochondrial membrane protein MTP18 in regulating mitochondrial fission.
- To elucidate the function of MTP18 in maintaining mitochondrial morphology.
Main Methods:
- Overexpression of human MTP18 in cultured cells.
- Co-expression with mitochondrial fusion (Mfn1) or dominant-negative fission (Drp1(K38A)) proteins.
- RNA interference (RNAi) to knockdown endogenous MTP18.
- Assessment of mitochondrial morphology using microscopy.
Main Results:
- Overexpression of MTP18 induced mitochondrial fragmentation, indicating increased fission.
- Mitochondrial fragmentation was suppressed by co-expressing Mfn1 or Drp1(K38A).
- MTP18 knockdown resulted in highly fused mitochondria, demonstrating its necessity for fission.
- MTP18 knockdown blocked fission induced by hFis1 overexpression.
Conclusions:
- MTP18 is a nuclear-encoded mitochondrial protein essential for regulating mitochondrial fission.
- MTP18 functions as an integral component of the mitochondrial division machinery.
- MTP18 plays a critical role in maintaining mitochondrial morphology through controlled fission events.
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