Regulation of mitochondrial morphology and cell survival by Mitogenin I and mitochondrial single-stranded DNA binding protein
Regulation of mitochondrial morphology and cell survival by Mitogenin I and mitochondrial single-stranded DNA binding protein
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DOI：
10.1016/j.bbagen.2006.05.012
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发表时间：
2006-09-01
影响因子：
3
通讯作者：
Higuti, Tomihiko
中科院分区：
文献类型：
--
作者：
Arakaki, Naokatu;Nishihama, Takeshi;Higuti, Tomihiko
我们发现，人类DNA聚合酶δ相互作用蛋白38的小鼠同源物，在本文中被称为丝裂原蛋白I，和线粒体单链DNA结合蛋白（mtSSB），被鉴定为幼年内脏脂肪变性小鼠心脏中的上调基因，在线粒体形态的调节中发挥作用。我们证明，在小鼠C2C12成肌细胞中，促分裂素I或mtSSB的过度表达分别增加了延长或破碎的线粒体。另一方面，通过RNA干扰沉默Mitogenin I或mtSSB分别导致细胞中片段化或伸长的线粒体增加，表明Mitogenin I和mtSSB分别参与线粒体融合和分裂的过程。此外，我们发现，丝裂原蛋白I的沉默导致台盼蓝阳性细胞的数量增加，mtSSB的沉默导致细胞对依托泊苷凋亡刺激的敏感性增强。目前的结果表明，这些蛋白质在细胞存活中发挥作用。(c)2006 Elsevier B.V保留所有权利。
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. (c) 2006 Elsevier B.V All rights reserved.