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Thioredoxin f1 and NADPH-dependent thioredoxin reductase C have overlapping functions in regulating photosynthetic metabolism and plant growth in response to varying light conditions

机译:硫氧还蛋白f1和NADPH依赖的硫氧还蛋白还原酶C在调节光照条件下具有重叠的调节光合作用代谢和植物生长的功能

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摘要

Two different thiol-redox-systems exist in plant chloroplasts, the ferredoxin-thioredoxin system, which depends of ferredoxin reduced by the photosynthetic electron-transport chain and, thus, of light, and the NADPH-dependent thioredoxin reductase C (NTRC) system, which relies on NADPH and thus may be linked to sugar metabolism in the dark. Previous studies suggested therefore that the two different systems may have different functions in plants. We now report that there is a previously unrecognized functional redundancy of thioredoxin-f1 and NTRC in regulating photosynthetic metabolism and growth. In Arabidopsis mutants, combined - but not single - deficiencies of thioredoxin-f1 and NTRC led to severe growth inhibition and perturbed light acclimation, accompanied by strong impairments of Calvin-Benson-cycle activity and starch accumulation. Light-activation of key-enzymes of these pathways, fructose-1,6-bisphosphatase and ADP-glucose pyrophosphorylase, was almost completely abolished. The subsequent increase in NADPH/NADP+ and ATP/ADP ratios led to increased nitrogen assimilation, NADP-malate dehydrogenase activation and light-vulnerability of photosystem I core-proteins. In an additional approach, reporter studies show that Trx f1 and NTRC proteins are both co-localized in the same chloroplast substructure. Results provide genetic evidence that light and NADPH dependent thiol-redox systems interact at the level of thioredoxin-f1 and NTRC to coordinately participate in the regulation of Calvin-Benson-cycle, starch metabolism and growth in response to varying light conditions.
机译:植物叶绿体中存在两种不同的硫醇-氧化还原系统:铁氧还蛋白-硫氧还蛋白系统,其依赖于光合作用电子传输链所还原的铁氧还蛋白,因此取决于光,以及依赖于NADPH的硫氧还蛋白还原酶C(NTRC)系统,它依赖于NADPH,因此可能与黑暗中的糖代谢有关。因此,先前的研究表明,两种不同的系统在植物中可能具有不同的功能。我们现在报告说,在调节光合作用的代谢和生长方面,硫氧还蛋白-f1和NTRC具有以前无法识别的功能冗余。在拟南芥突变体中,硫氧还蛋白-f1和NTRC的综合缺陷(而非单一缺陷)导致严重的生长抑制和光适应,同时严重损害了Calvin-Benson循环活性和淀粉积累。这些途径的关键酶,果糖-1,6-双磷酸酶和ADP-葡萄糖焦磷酸化酶的光激活作用几乎被完全消除。随后NADPH / NADP +和ATP / ADP比率的增加导致氮同化作用增强,NADP-苹果酸脱氢酶活化和光系统I核心蛋白的光弱性。在另一种方法中,记者研究表明Trx f1和NTRC蛋白都共定位在同一叶绿体亚结构中。结果提供了遗传证据,表明依赖于光和NADPH的硫醇-氧化还原系统在硫氧还蛋白-f1和NTRC的水平上相互作用,以响应不同的光照条件,协调参与加尔文-本森循环,淀粉代谢和生长的调节。

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