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Life without complex I: proteome analyses of an Arabidopsis mutant lacking the mitochondrial NADH dehydrogenase complex

机译:没有复合体的生活I:缺乏线粒体NADH脱氢酶复合体的拟南芥突变体的蛋白质组分析

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Complex I dysfunction causes reorganization of cellular respiration and affects metabolic processes in mitochondria, plastids, peroxisomes, and other cellular compartments with drastic consequences for growth and development.The mitochondrial NADH dehydrogenase complex (complex I) is of particular importance for the respiratory chain in mitochondria. It is the major electron entry site for the mitochondrial electron transport chain (mETC) and therefore of great significance for mitochondrial ATP generation. We recently described an Arabidopsis thaliana double-mutant lacking the genes encoding the carbonic anhydrases CA1 and CA2, which both form part of a plant-specific 'carbonic anhydrase domain' of mitochondrial complex I. The mutant lacks complex I completely. Here we report extended analyses for systematically characterizing the proteome of the ca1ca2 mutant. Using various proteomic tools, we show that lack of complex I causes reorganization of the cellular respiration system. Reduced electron entry into the respiratory chain at the first segment of the mETC leads to induction of complexes II and IV as well as alternative oxidase. Increased electron entry at later segments of the mETC requires an increase in oxidation of organic substrates. This is reflected by higher abundance of proteins involved in glycolysis, the tricarboxylic acid cycle and branched-chain amino acid catabolism. Proteins involved in the light reaction of photosynthesis, the Calvin cycle, tetrapyrrole biosynthesis, and photorespiration are clearly reduced, contributing to the significant delay in growth and development of the double-mutant. Finally, enzymes involved in defense against reactive oxygen species and stress symptoms are much induced. These together with previously reported insights into the function of plant complex I, which were obtained by analysing other complex I mutants, are integrated in order to comprehensively describe 'life without complex I'.
机译:复合物I功能障碍导致细胞呼吸重组,并影响线粒体,质体,过氧化物酶体和其他细胞区室的代谢过程,对生长发育产生重大影响。线粒体NADH脱氢酶复合物(复合物I)对于线粒体呼吸链特别重要。它是线粒体电子传输链(mETC)的主要电子进入位点,因此对于线粒体ATP的产生具有重要意义。我们最近描述了拟南芥双突变体,缺少编码碳酸酐酶CA1和CA2的基因,两者均构成线粒体复合体I的植物特异性“碳酸酐酶结构域”的一部分。该突变体完全缺乏复合体I。在这里,我们报告扩展的分析,以系统地表征ca1ca2突变体的蛋白质组。使用各种蛋白质组学工具,我们表明缺乏复杂的I导致细胞呼吸系统的重组。电子在mETC的第一部分进入呼吸链的减少会导致复合物II和IV以及其他氧化酶的诱导。在mETC的后段增加的电子进入需要增加有机底物的氧化。这反映在糖酵解,三羧酸循环和支链氨基酸分解代谢中的蛋白质含量更高。光合作用,加尔文循环,四吡咯生物合成和光呼吸的光反应中涉及的蛋白质明显减少,从而导致双突变体生长和发育的显着延迟。最后,与活性氧防御和压力症状防御有关的酶被大量诱导。这些与以前报道的对植物复合物I功能的见解(通过分析其他复合物I突变体获得)相结合,以全面描述“没有复合物I的生活”。

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