Cardiolipin stabilizes respiratory chain supercomplexes
Cardiolipin stabilizes respiratory chain supercomplexes
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DOI：
10.1074/jbc.m308366200
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发表时间：
2003-12-26
影响因子：
4.8
通讯作者：
Schägger, H
中科院分区：
文献类型：
--
作者：
Pfeiffer, K;Gohil, V;Schägger, H
心磷脂稳定的酿酒酵母呼吸链复合物III和IV（泛醇：细胞色素c氧化还原酶和细胞色素c氧化酶，分别）的超复合物，但不是必不可少的，因为他们也被发现在线粒体内膜的心磷脂缺陷株。用心磷脂重建在很大程度上恢复了野生型稳定性。复合物III和IV的假定界面包括细胞色素B和c（1）的跨膜螺旋和紧密结合的心磷脂。亚基Rip 1 p，Qcr 6p，Qcr 9 p，Qcr 10 p，Cox 8 p，Cox 12 p和Cox 13 p和细胞色素c不是组装超复合物所必需的;在没有Qcr 6p的情况下，甚至促进了超复合物的形成。心磷脂的另一个显著作用与细胞色素c氧化酶有关。我们发现，心磷脂缺陷株窝藏几乎不活跃的静息细胞色素c氧化酶的膜。转换到完全激活的脉冲状态发生在一分钟的时间尺度上。
Cardiolipin stabilized supercomplexes of Saccharomyces cerevisiae respiratory chain complexes III and IV (ubiquinol: cytochrome c oxidoreductase and cytochrome c oxidase, respectively), but was not essential for their formation in the inner mitochondrial membrane because they were found also in a cardiolipin-deficient strain. Reconstitution with cardiolipin largely restored wild-type stability. The putative interface of complexes III and IV comprises transmembrane helices of cytochromes b and c(1) and tightly bound cardiolipin. Subunits Rip1p, Qcr6p, Qcr9p, Qcr10p, Cox8p, Cox12p, and Cox13p and cytochrome c were not essential for the assembly of supercomplexes; and in the absence of Qcr6p, the formation of supercomplexes was even promoted. An additional marked effect of cardiolipin concerns cytochrome c oxidase. We show that a cardiolipin-deficient strain harbored almost inactive resting cytochrome c oxidase in the membrane. Transition to the fully active pulsed state occurred on a minute time scale.