Patil Priyanka Pradeep, Kodru Sandeesha, Szabó Milán, Vass Imre
Institute of Plant Biology, HUN-REN Biological Research Centre, Szeged, Hungary.
Doctoral School of Biology, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
Physiol Plant. 2025 Jan-Feb;177(1):e70066. doi: 10.1111/ppl.70066.
Cyanobacteria are important model organisms for studying the process of photosynthesis and the effects of environmental stress factors. This study aimed to identify the inhibitory sites of NaCl in the whole photosynthetic electron transport in Synechocystis sp. PCC 6803 WT cells by using multiple biophysical tools. Exposure of cells to various NaCl concentrations (200 mM to 1 M) revealed the inhibition of Photosystem II (PSII) activity at the water oxidizing complex and between the Q and Q electron acceptors. In contrast to the inhibition of PSII, electron flow through Photosystem I (PSI) was accelerated, indicating enhanced cyclic electron flow. The oxygen-evolving capacity of the cells was inhibited to a larger extent when only CO was the final electron acceptor in the Calvin-Benson-Bassham (CBB) cycle than in the presence of the PSII electron acceptor DMBQ, suggesting important NaCl inhibitory site(s) downstream of PSI. Measurements of NADPH kinetics revealed NaCl-induced inhibition of light-induced production of NADPH as well as retardation of NADPH consumption both in the light and in the initial dark period after switching off the light. Chlorophyll fluorescence kinetics, measured in parallel with NADPH fluorescence, showed the enhancement of post-illumination fluorescence rise up to 500 mM NaCl, which was however inhibited at higher NaCl concentrations. Our results show, for the first time, that NaCl inhibits the activity of the CBB cycle at least at two different sites, and confirm earlier results about the NaCl-induced inhibition of the PSII donor and acceptor side and the enhancement of electron flow through PSI.
蓝细菌是研究光合作用过程和环境胁迫因子影响的重要模式生物。本研究旨在通过使用多种生物物理工具，确定NaCl在集胞藻PCC 6803野生型细胞整个光合电子传递中的抑制位点。将细胞暴露于不同浓度的NaCl（200 mM至1 M）下，结果表明在水氧化复合物以及Q和Q电子受体之间，光系统II（PSII）的活性受到抑制。与PSII的抑制相反，通过光系统I（PSI）的电子流加速，表明循环电子流增强。当卡尔文-本森-巴斯姆（CBB）循环中仅CO作为最终电子受体时，细胞的放氧能力比存在PSII电子受体DMBQ时受到更大程度的抑制，这表明在PSI下游存在重要的NaCl抑制位点。NADPH动力学测量结果显示，NaCl会抑制光诱导的NADPH生成，以及在光照期间和光照关闭后的初始黑暗期NADPH的消耗延迟。与NADPH荧光同时测量的叶绿素荧光动力学表明，在高达500 mM NaCl的浓度下，光照后荧光上升增强，但在更高的NaCl浓度下受到抑制。我们的结果首次表明，NaCl至少在两个不同位点抑制CBB循环的活性，并证实了先前关于NaCl诱导的PSII供体侧和受体侧抑制以及通过PSI的电子流增强的结果。
