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氮氧化物在 S-饥饿时重塑光合作用器官

Nitric Oxide Remodels the Photosynthetic Apparatus upon S-Starvation in .

机构信息

Laboratoire de Physiologie Membranaire et Moléculaire du Chloroplaste, Centre National de la Recherche Scientifique, Sorbonne Université, Institut de Biologie Physico-Chimique, 75005 Paris, France.

Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Centre National de la Recherche Scientifique, Sorbonne Université, Institut de Biologie Physico-Chimique, 75005 Paris, France.

出版信息

Plant Physiol. 2019 Feb;179(2):718-731. doi: 10.1104/pp.18.01164. Epub 2018 Dec 10.

Abstract

Many photosynthetic autotrophs have evolved responses that adjust their metabolism to limitations in nutrient availability. Here we report a detailed characterization of the remodeling of photosynthesis upon sulfur starvation under heterotrophy and photo-autotrophy in the green alga (). Photosynthetic inactivation under low light and darkness is achieved through specific degradation of Rubisco and cytochrome and occurs only in the presence of reduced carbon in the medium. The process is likely regulated by nitric oxide (NO), which is produced 24 h after the onset of starvation, as detected with NO-sensitive fluorescence probes visualized by fluorescence microscopy. We provide pharmacological evidence that intracellular NO levels govern this degradation pathway: the addition of a NO scavenger decreases the rate of cytochrome and Rubisco degradation, whereas NO donors accelerate the degradation. Based on our analysis of the relative contribution of the different NO synthesis pathways, we conclude that the NO-dependent nitrate reductase-independent pathway is crucial for NO production under sulfur starvation. Our data argue for an active role for NO in the remodeling of thylakoid protein complexes upon sulfur starvation.

摘要

许多光合作用自养生物已经进化出了相应的反应,可以根据养分供应的限制来调整其新陈代谢。在这里,我们报道了在异养和自养条件下,绿藻()中硫饥饿时光合作用重构的详细特征。在低光照和黑暗下,光合失活是通过 Rubisco 和细胞色素 的特异性降解来实现的,而且只有在培养基中存在还原态碳时才会发生。这个过程可能受到一氧化氮(NO)的调控,NO 在饥饿开始后 24 小时产生,可以通过荧光显微镜观察到用 NO 敏感荧光探针可视化检测到。我们提供了药理学证据表明,细胞内的 NO 水平控制着这条降解途径:添加 NO 清除剂会降低细胞色素 和 Rubisco 降解的速度,而 NO 供体则会加速降解。基于我们对不同的 NO 合成途径相对贡献的分析,我们得出结论,在硫饥饿时,NO 依赖性硝酸还原酶非依赖性途径对于 NO 的产生至关重要。我们的数据表明,在硫饥饿时,NO 可主动参与类囊体蛋白复合物的重构。

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