FMP30 is required for the maintenance of a normal cardiolipin level and mitochondrial morphology in the absence of mitochondrial phosphatidylethanolamine synthesis
FMP30 is required for the maintenance of a normal cardiolipin level and mitochondrial morphology in the absence of mitochondrial phosphatidylethanolamine synthesis
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DOI：
10.1111/j.1365-2958.2011.07569.x
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发表时间：
2011-04-01
影响因子：
3.6
通讯作者：
Kuge, Osamu
中科院分区：
文献类型：
--
作者：
Kuroda, Takuya;Tani, Motohiro;Kuge, Osamu
酿酒酵母（Saccharomycescerevisiae）线粒体中含有Crd1p和Psd1p酶，分别合成心磷脂（CL）和磷脂酰乙醇胺。先前的研究表明，crd 1 Delta与psd 1 Delta具有合成致死性。在这项研究中，要确定新的基因参与CL代谢，我们寻找基因与Psd1p的相互作用，并发现，FMP30编码线粒体内膜蛋白的缺失导致合成的生长缺陷与psd 1 δ。虽然fmp 30 Delta细胞正常生长并显示出CL水平略微降低，但与野生型对照相比，fmp 30 Delta psd 1 Delta细胞显示出严重的生长缺陷和CL水平降低约20倍。我们还发现，FMP30的缺失导致线粒体形态的缺陷。此外，FMP30与7个线粒体形态基因相互作用。这些结果表明，Fmp30 p参与线粒体形态的维持，并且在线粒体磷脂酰乙醇胺合成不存在的情况下，为正常水平CL的积累所需。
P>Mitochondria of the yeast Saccharomyces cerevisiae contain enzymes Crd1p and Psd1p, which synthesize cardiolipin (CL) and phosphatidylethanolamine respectively. A previous study indicated that crd1 Delta is synthetically lethal with psd1 Delta. In this study, to identify novel genes involved in CL metabolism, we searched for genes that genetically interact with Psd1p, and found that deletion of FMP30 encoding a mitochondrial inner membrane protein results in a synthetic growth defect with psd1 Delta. Although fmp30 Delta cells grew normally and exhibited a slightly decreased CL level, fmp30 Delta psd1 Delta cells exhibited a severe growth defect and an about 20-fold reduction in the CL level, as compared with the wild-type control. We found also that deletion of FMP30 caused a defect in mitochondrial morphology. Furthermore, FMP30 genetically interacted with seven mitochondrial morphology genes. These results indicated that Fmp30p is involved in the maintenance of mitochondrial morphology and required for the accumulation of a normal level of CL in the absence of mitochondrial phosphatidylethanolamine synthesis.