Search

Mitochondria are highly dynamic organelles in eukaryotic cells. Although the role of mitochondria in metabolism, ATP production and apoptosis is more widely recognized, alterations in mitochondrial morphology and abundance are also important for cellular functions. Here we investigated mitochondrial dynamics in synchronized HeLa cells in which the major stages of the cell cycle of the observed cells were resolved by staining phosphorylate histones H1 and H3, and showed that mitochondria exist as filamentous network structures throughout the cell cycle progression, changing their morphology, distribution, and abundance. The current results suggest that mitochondrial condensation occurred at prophase is required for the proper progression of mitochondrial division.

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.