Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1948729 | Biochimica et Biophysica Acta (BBA) - General Subjects | 2006 | 9 Pages |
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.
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Authors
Naokatu Arakaki, Takeshi Nishihama, Akira Kohda, Hiroyuki Owaki, Yoshinori Kuramoto, Reika Abe, Toshiyuki Kita, Midori Suenaga, Toshiki Himeda, Masamichi Kuwajima, Hirofumi Shibata, Tomihiko Higuti,