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

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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