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Updated: Aug 7, 2026

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
Published on: November 14, 2025
Regulation of mitochondrial morphology and cell survival by Mitogenin I and mitochondrial single-stranded DNA binding
Naokatu Arakaki1, Takeshi Nishihama, Akira Kohda
1Department of Molecular Cell Biology and Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8505, Japan. arakaki@ph.tokushima-u.ac.jp
Abstract:
We found that a mouse homolog of human DNA polymerase delta interacting protein 38, referred to as Mitogenin I in this paper, and mitochondrial single-stranded DNA-binding protein (mtSSB), identified as upregulated genes in the heart of mice with juvenile visceral steatosis, play a role in the regulation of mitochondrial morphology. We demonstrated that overexpression of Mitogenin I or mtSSB increased elongated or fragmented mitochondria in mouse C2C12 myoblast cells, respectively. On the other hand, the silencing of Mitogenin I or mtSSB by RNA interference led to an increase in fragmented or elongated mitochondria in the cells, respectively, suggesting that Mitogenin I and mtSSB are involved in the processes of mitochondrial fusion and fission, respectively. In addition, we showed that the silencing of Mitogenin I resulted in an increase in the number of trypan blue-positive cells and the silencing of mtSSB resulted in an enhancement of the sensitivity of the cells to apoptotic stimulation by etoposide. The present results demonstrated that these proteins play a role in cell survival.
Insights
Mitogenin I and mitochondrial single-stranded DNA-binding protein (mtSSB) regulate mitochondrial shape and are crucial for cell survival. Their dysfunction impacts mitochondrial fusion and fission, affecting cell health.
Area of Science:
- Cell Biology
- Mitochondrial Biology
- Molecular Biology
Background:
- Juvenile visceral steatosis in mice shows upregulated genes in heart tissue.
- Mitogenin I (mouse homolog of human DNA polymerase delta interacting protein 38) and mtSSB are implicated in cellular processes.
Purpose of the Study:
- To investigate the role of Mitogenin I and mtSSB in mitochondrial morphology and cell survival.
- To determine the involvement of these proteins in mitochondrial fusion and fission.
Main Methods:
- Overexpression and RNA interference (silencing) of Mitogenin I and mtSSB in mouse C2C12 myoblast cells.
- Analysis of mitochondrial morphology (elongated vs. fragmented).
- Assessment of cell viability using trypan blue staining and sensitivity to etoposide-induced apoptosis.
Main Results:
- Overexpression of Mitogenin I led to elongated mitochondria; overexpression of mtSSB led to fragmented mitochondria.
- Silencing Mitogenin I caused fragmented mitochondria; silencing mtSSB caused elongated mitochondria, indicating roles in fusion and fission respectively.
- Mitogenin I silencing increased cell death, while mtSSB silencing enhanced apoptosis sensitivity, highlighting their roles in cell survival.
Conclusions:
- Mitogenin I and mtSSB are key regulators of mitochondrial morphology, influencing both fusion and fission dynamics.
- These proteins are essential for maintaining cell survival and protecting against apoptosis.
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