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首页> 外文期刊>The Plant Cell >From Endoplasmic Reticulum to Mitochondria: Absence of the Arabidopsis ATP Antiporter Endoplasmic Reticulum Adenylate Transporter1 Perturbs Photorespiration
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From Endoplasmic Reticulum to Mitochondria: Absence of the Arabidopsis ATP Antiporter Endoplasmic Reticulum Adenylate Transporter1 Perturbs Photorespiration

机译:从内质网到线粒体:亚洲偶联患者的缺失ATP抗紫杉醇内质网腺苷转运蛋白腺苷酸1 perturbs光素

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摘要

The carrier Endoplasmic Reticulum Adenylate Transporter1 (ER-ANT1) resides in the endoplasmic reticulum (ER) membrane and acts as an ATP/ADP antiporter. Mutant plants lacking ER-ANT1 exhibit a dwarf phenotype and their seeds contain reduced protein and lipid contents. In this study, we describe a further surprising metabolic peculiarity of the er-ant1 mutants. Interestingly, Gly levels in leaves are immensely enhanced (263) when compared with that of wild-type plants. Gly accumulation is caused by significantly decreased mitochondrial glycine decarboxylase (GDC) activity. Reduced GDC activity in mutant plants was attributed to oxidative posttranslational protein modification induced by elevated levels of reactive oxygen species (ROS). GDC activity is crucial for photorespiration; accordingly, morphological and physiological defects in er-ant1 plants were nearly completely abolished by application of high environmental CO2 concentrations. The latter observation demonstrates that the absence of ER-ANT1 activity mainly affects photorespiration (maybe solely GDC), whereas basic cellular metabolism remains largely unchanged. Since ER-ANT1 homologs are restricted to higher plants, it is tempting to speculate that this carrier fulfils a plant-specific function directly or indirectly controlling cellular ROS production. The observation that ER-ANT1 activity is associated with cellular ROS levels reveals an unexpected and critical physiological connection between the ER and other organelles in plants.
机译:载体内质网腺苷转运蛋白转运蛋白(ER-ANT1)位于内质网(ER)膜中,并用作ATP / ADP抗原膜。缺乏ER-ANT1的突变植物表现出矮化表型及其种子含有降低的蛋白质和脂质含量。在这项研究中,我们描述了ER-ANT1突变体的进一步令人惊讶的代谢特性。有趣的是,与野生型植物相比,叶片中的糖水平均增强(263)。通过显着降低的线粒体甘氨酸脱羧酶(GDC)活性,累积累积。突变植物中的GDC活性降低归因于通过升高的反应性氧(ROS)诱导的氧化发生蛋白质改性。 GDC活性对于光抑制至关重要;因此,通过施加高环境CO 2浓度,ER-ANT1植物中的形态学和生理缺陷几乎完全被废除。后一种观察表明,没有ER-ANT1活性的情况主要影响光孔(可能是GDC),而碱性细胞代谢仍然很大程度上不变。由于ER-ANT1同源物仅限于高等植物,因此推测该载体直接或间接控制细胞ROS生产的植物特异性功能。 ER-ANT1活性与细胞ROS水平相关的观察结果揭示了植物中ER和其他细胞器之间的意外和批判的生理联系。

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  • 来源
    《The Plant Cell》 |2013年第7期|共14页
  • 作者单位

    Univ Kaiserslautern Dept Plant Physiol D-67663 Kaiserslautern Germany;

    Univ Kaiserslautern Dept Plant Physiol D-67663 Kaiserslautern Germany;

    Univ Kaiserslautern Dept Plant Physiol D-67663 Kaiserslautern Germany;

    Univ Kaiserslautern Dept Plant Physiol D-67663 Kaiserslautern Germany;

    Univ Rostock Dept Plant Physiol D-18059 Rostock Germany;

    Univ Rostock Dept Plant Physiol D-18059 Rostock Germany;

    Univ Kaiserslautern Dept Cell Biochem D-67663 Kaiserslautern Germany;

    Univ Kaiserslautern Dept Cell Biol D-67663 Kaiserslautern Germany;

    Univ Kaiserslautern Dept Plant Physiol D-67663 Kaiserslautern Germany;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 植物细胞学;
  • 关键词

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