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首页> 美国卫生研究院文献>Antioxidants >The Phosphofructokinase Isoform AtPFK5 Is a Novel Target of Plastidic Thioredoxin-f-Dependent Redox Regulation
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The Phosphofructokinase Isoform AtPFK5 Is a Novel Target of Plastidic Thioredoxin-f-Dependent Redox Regulation

机译：磷酸氨基氨基族同样ATPFK5是血浆培养六氧化酶-F依赖性氧化还原调控的新靶标

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The chloroplast primary metabolism is of central importance for plant growth and performance. Therefore, it is tightly regulated in order to adequately respond to multiple environmental conditions. A major fluctuation that plants experience each day is the change between day and night, i.e., the change between assimilation and dissimilation. Among other mechanisms, thioredoxin-mediated redox regulation is an important component of the regulation of plastid-localized metabolic enzymes. While assimilatory processes such as the Calvin–Benson cycle are activated under illumination, i.e., under reducing conditions, carbohydrate degradation is switched off during the day. Previous analyses have identified enzymes of the oxidative pentose phosphate pathway to be inactivated by reduction through thioredoxins. In this work, we present evidence that an enzyme of the plastidic glycolysis, the phosphofructokinase isoform AtPFK5, is also inactivated through reduction by thioredoxins, namely by thioredoxin-f. With the help of chemical oxidation, mutant analyses and further experiments, the highly conserved motif CXDXXC in AtPFK5 was identified as the target sequence for this regulatory mechanism. However, knocking out this isoform in plants had only very mild effects on plant growth and performance, indicating that the complex primary metabolism in plants can overcome a lack in AtPFK5 activity.
机译：叶绿体初级代谢对植物生长和性能具有核心重要性。因此，它是紧密调节的，以便充分响应多种环境条件。每天植物经历的主要波动是白天和夜间的变化，即同化和异化之间的变化。在其他机制之外，肝素介导的氧化还原调节是体积局部化代谢酶调节的重要组成部分。虽然在照明下激活诸如Calvin-Benson循环的同化过程，但在还原条件下，在白天关闭碳水化合物降解。先前的分析已经确定氧化戊糖磷酸磷酸盐途径的酶，通过通过硫辛还原而灭活。在这项工作中，我们提出了一种证据，证据表明，磷化吡啶氨酸异族ATPFK5的血压糖酵解的酶也通过硫辛素的还原，即通过硫辛蛋白-F来灭活。借助化学氧化，突变分析和进一步实验，鉴定了ATPFK5中的高度保守的基序CXDXXC作为该调节机制的靶序列。然而，淘汰植物中的这种同种型对植物生长和性能影响非常轻微，表明植物中的复杂原发性代谢可以克服ATPFK5活性缺乏。

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