ミトコンドリアのダイナミクスを制御する新規因子の解明

抄録

  Mitochondria are highly dynamic organelles and undergo continuous fission and fusion events in physiological situations. It was observed that mitochondrial morphology and number are changed in living cells during cellular differentiation, development, and under pathological conditions including muscle dystrophy, cardiomyopathy, and cancer. Defined sets of proteins are known to mediate mitochondrial fission and fusion and to constitute regulatory components controlling mitochondrial dynamics. In the present study, we first investigated mitochondrial dynamics during the cell cycle progression, and found that mitochondria exist as filamentous network structures throughout the cell cycle progression, changing their morphology, distribution, and abundance. In addition, we found that a mouse homolog of human DNA polymerase delta interacting protein 38, referred to as Mitogenin I, 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.