Functional analysis of AAA ATPase Cdc48p on regulation of mitochondrial morphology

线粒体经过不断的融合和裂变，保持动态的管状形态。我们已经证明，Cdc48p（一种细胞质AAA伴侣蛋白）的功能缺失突变可诱导线粒体聚集。进一步的分析显示，线粒体融合似乎在Cdc48p突变体中受到干扰。此外，我们探索了与Cdc48p一起调控线粒体形态的伙伴蛋白，发现Shp1p的缺失导致线粒体形态异常。这些结果表明，Cdc48p-Shp1p复合物调节线粒体融合事件。

Mitochondria undergo continuous fusion and fission, which maintain dynamic tubular morphology. We have shown that loss-of-function mutations of Cdc48p, a cytosolic AAA chaperone, induce mitochondrial aggregation. Further analyses revealed that mitochondrial fusion seems to be perturbed in Cdc48p mutants. Moreover, we explored partner proteins functioning together with Cdc48p in mitochondrial morphology regulation, and found that deletion of Shp1p induces aberrant mitochondrial morphology. These results suggests that the Cdc48p-Shp1p complex regulates the mitochondrial fusion event.