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高光适应机制在 PsbS 敲除拟南芥突变体中缺失。

High Light Acclimation Mechanisms Deficient in a PsbS-Knockout Arabidopsis Mutant.

机构信息

Department of Integrated Biological Science, Department of Molecular Biology, Pusan National University, Busan 46241, Korea.

Graduate Department of Life and Pharmaceutical Sciences, Center for Cell Signaling & Drug Discovery Research, Ewha Womans University, Seoul 03760, Korea.

出版信息

Int J Mol Sci. 2022 Feb 28;23(5):2695. doi: 10.3390/ijms23052695.

DOI:10.3390/ijms23052695
PMID:35269832
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8910700/
Abstract

The photosystem II PsbS protein of thylakoid membranes is responsible for regulating the energy-dependent, non-photochemical quenching of excess chlorophyll excited states as a short-term mechanism for protection against high light (HL) stress. However, the role of PsbS protein in long-term HL acclimation processes remains poorly understood. Here we investigate the role of PsbS protein during long-term HL acclimation processes in wild-type (WT) and mutants of which lack the PsbS protein. During long-term HL illumination, photosystem II photochemical efficiency initially dropped, followed by a recovery of electron transport and photochemical quenching (qL) in WT, but not in mutants. In addition, we observed a reduction in light-harvesting antenna size during HL treatment that ceased after HL treatment in WT, but not in mutants. When plants were adapted to HL, more reactive oxygen species (ROS) were accumulated in mutants compared to WT. Gene expression studies indicated that mutants failed to express genes involved in plastoquinone biosynthesis. These results suggest that the PsbS protein regulates recovery processes such as electron transport and qL during long-term HL acclimation by maintaining plastoquinone biosynthetic gene expression and enhancing ROS homeostasis.

摘要

类囊体膜中的光系统 II PsbS 蛋白负责调节依赖于能量的、过量叶绿素激发态的非光化学猝灭,作为一种短期机制来防止高光(HL)胁迫。然而,PsbS 蛋白在长期 HL 适应过程中的作用仍知之甚少。在这里,我们研究了 PsbS 蛋白在野生型(WT)和缺乏 PsbS 蛋白的突变体 中在长期 HL 适应过程中的作用。在长期 HL 照射下,光系统 II 光化学效率最初下降,随后在 WT 中电子传递和光化学猝灭(qL)恢复,但在 突变体中没有恢复。此外,我们观察到在 HL 处理过程中,在 WT 中,光捕获天线的大小减小,但在 突变体中没有。当植物适应 HL 时,与 WT 相比, 突变体中积累了更多的活性氧(ROS)。基因表达研究表明, 突变体未能表达参与质醌生物合成的基因。这些结果表明,PsbS 蛋白通过维持质醌生物合成基因的表达和增强 ROS 平衡来调节电子传递和 qL 等恢复过程,从而在长期 HL 适应过程中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf9/8910700/a2669a824e7e/ijms-23-02695-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf9/8910700/a2669a824e7e/ijms-23-02695-g009.jpg
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