REORGANIZATION OF HELA-CELL CYTOSKELETON INDUCED BY AN UNCOUPLER OF OXIDATIVE-PHOSPHORYLATION
REORGANIZATION OF HELA-CELL CYTOSKELETON INDUCED BY AN UNCOUPLER OF OXIDATIVE-PHOSPHORYLATION
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DOI：
10.1038/295334a0
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发表时间：
1982-01-01
期刊：
影响因子：
64.8
通讯作者：
BORNENS, M
中科院分区：
文献类型：
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作者：
MARO, B;BORNENS, M
线粒体和微管之间的关联已经从显微镜研究1,2和线粒体的细胞重新分配被秋碱诱导，破坏微管1。中间纤维也被认为与线粒体相互作用。为了进一步研究这种关联，我们现在研究了三种代谢抑制剂诱导的线粒体功能损伤对细胞骨架的影响：抑制电子传递的叠氮化钠；寡霉素，抑制ATP合成酶；羰基氰基-三氟甲氧基苯基腙（FCCP），一种质子离子载体，能使ATP合成过程中的电子传递不耦合。我们发现用FCCP处理细胞会导致微管的破坏和静脉蛋白丝的聚集。这种效应不是由线粒体ATP耗竭引起的，但可能与另一个与线粒体电化学梯度快速耗散有关的事件有关。
An association between mitochondria and microtubules has been suggested from microscopic studies1,2and by the cellular redistribution of mitochondria that is induced by colcemid, which disrupts microtubules1. Intermediate filaments have also been proposed to interact with mitochondria1. To investigate this association further, we have now studied the effect on the cytoskeleton of impairment of mitochondrial functions induced by three metabolic inhibitors: sodium azide, which inhibits electron transport; oligomycin, which inhibits ATP synthetase; and carbonylcyanidep-trifluoromethoxyphenylhydrazone (FCCP), a proton ionophore which uncouples electron transport from ATP synthesis. We have found that treatment of cells with FCCP leads to a disruption of microtubules and an aggregation of vimentin filaments. This effect is not provoked by mitochondrial ATP depletion, but could be linked to another event related to the rapid dissipation of the mitochondrial electrochemical gradient.