Division versus fusion: Dnm1p and Fzo1p antagonistically regulate mitochondrial shape.

Division versus fusion: Dnm1p and Fzo1p antagonistically regulate mitochondrial shape.
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DOI:
10.1083/jcb.147.4.699
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发表时间:
1999-11-15
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Jensen RE
Jensen RE
中科院分区:
其他
文献类型:
--
作者:
Sesaki H;Jensen RE

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在酵母中,线粒体的分裂和融合在生长、交配和孢子形成过程中受到高度调控,但控制这些活动的机制尚不清楚。使用一种新的筛选方法,我们分离出线粒体失去正常结构的突变体,转而形成一个巨大的相互连接的小管网络。这些突变体似乎在线粒体分裂方面存在缺陷,它们都携带着DNM1的突变,DNM1是一种定位于线粒体的动力蛋白相关蛋白。我们还分离了含有大量线粒体片段的突变体。这些突变体在FZO1基因上存在缺陷,FZO1基因以前被证明是线粒体融合所必需的。令人惊讶的是,我们发现在DNM1 fzo1双突变体中,正常的线粒体形状恢复了。在DNM1fzo1细胞中诱导Dnm1p的表达导致线粒体迅速碎裂。我们认为DNM1突变体在线粒体分裂方面存在缺陷,线粒体分裂是一种对抗融合的活性。因此,我们的结果表明,线粒体的形状通常受分裂和融合之间的平衡控制,这分别需要Dnm1p和Fzo1p。
In yeast, mitochondrial division and fusion are highly regulated during growth, mating and sporulation, yet the mechanisms controlling these activities are unknown. Using a novel screen, we isolated mutants in which mitochondria lose their normal structure, and instead form a large network of interconnected tubules. These mutants, which appear defective in mitochondrial division, all carried mutations in DNM1, a dynamin-related protein that localizes to mitochondria. We also isolated mutants containing numerous mitochondrial fragments. These mutants were defective in FZO1, a gene previously shown to be required for mitochondrial fusion. Surprisingly, we found that in dnm1 fzo1 double mutants, normal mitochondrial shape is restored. Induction of Dnm1p expression in dnm1 fzo1 cells caused rapid fragmentation of mitochondria. We propose that dnm1 mutants are defective in the mitochondrial division, an activity antagonistic to fusion. Our results thus suggest that mitochondrial shape is normally controlled by a balance between division and fusion which requires Dnm1p and Fzo1p, respectively.
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