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线粒体内能量耗竭细胞的生长缺陷:线粒体生物发生的作用

Growth defects in intramitochondrial energy depleted cells: role of mitochondrial biogenesis.

作者信息

Hapala L

机构信息

Institute of Animal Physiology, Slovak Academy of Sciences, Ivanka pri Dunaji, Czechoslovakia.

出版信息

Biochem Biophys Res Commun. 1989 Mar 15;159(2):612-7. doi: 10.1016/0006-291x(89)90038-7.

Abstract

Simultaneous inhibition of oxidative phosphorylation by rho- mutation and adenine nucleotide exchange by op1 mutation or bongkrekic acid results in intramitochondrial energy depletion and cessation of growth in yeast. Effect of energy depletion of mitochondria on mitochondrial biogenesis was studied in intact yeast cells. Immunoblot analysis revealed an overall decrease in cellular content of two mitochondrial proteins - ADP/ATP translocase and beta subunit of mitochondrial ATPase - together with their lower ability to reach the proper intramitochondrial compartment. Both effects indicate disturbed biogenesis of energy depleted mitochondria. Quantitative differences in growth abilities and mitochondrial damage observed in two studied systems - op1 rho- double mutants and rho- cells treated with bongkrekic acid - can be explained by different degree of intramitochondrial energy depletion due to leakiness of op1 mutation in op1 rho- cells.

摘要

rho突变对氧化磷酸化的同时抑制以及op1突变或 Bongkrekic 酸对腺嘌呤核苷酸交换的抑制,会导致酵母线粒体内能量耗竭和生长停止。在完整的酵母细胞中研究了线粒体能量耗竭对线粒体生物发生的影响。免疫印迹分析显示,两种线粒体蛋白——ADP/ATP转位酶和线粒体ATP酶的β亚基——的细胞含量总体下降,同时它们进入线粒体内适当区室的能力也较低。这两种效应都表明能量耗竭的线粒体生物发生受到干扰。在两个研究系统——op1 rho-双突变体和用 Bongkrekic 酸处理的rho-细胞——中观察到的生长能力和线粒体损伤的定量差异,可以通过op1 rho-细胞中op1突变的渗漏导致的线粒体内能量耗竭程度不同来解释。

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