Zhao J D, Brand J J
Department of Botany, University of Texas, Austin 78713.
Arch Biochem Biophys. 1988 Aug 1;264(2):657-64. doi: 10.1016/0003-9861(88)90332-3.
Incubation of Synechocystis PCC 6714 in liquid medium devoid of Na+ results in a light-dependent loss in photosynthetic O2 evolving capacity within 1 h. Photosynthetic activity is fully restored and normal growth resumes after Na+ is supplied to culture medium of depleted cells. If external Na+ is provided as soon as inhibition becomes complete, normal photosynthesis is restored within 3 min. However, if cells are further illuminated for several h under Na+ stress, then full recovery takes much longer, and requires new protein synthesis. Electron transport assays using isolated membranes demonstrate that the immediate inhibition resulting from Na+ depletion involves the O2 evolving site, while the secondary effect requiring new protein synthesis occurs near the reaction center of Photosystem II. Experiments conducted at different pH values and in the absence of inorganic carbon demonstrate that within the short time duration of these experiments Na+ does not inhibit photosynthesis by restricting bicarbonate movement into the cells. These experiments extend previous results with other cyanobacteria which demonstrated that Ca2+ and Na+ stress cause reversible damage at a site near the reaction center of Photosystem II. The damage can be characterized as a primary ion effect at the oxygen evolving site and a secondary photoinhibition near the reaction center of Photosystem II.
将集胞藻PCC 6714在无Na⁺的液体培养基中培养,1小时内光合放氧能力会出现光依赖性损失。向耗尽细胞的培养基中供应Na⁺后,光合活性完全恢复,正常生长恢复。如果在抑制完全后立即提供外部Na⁺,3分钟内即可恢复正常光合作用。然而,如果细胞在Na⁺胁迫下进一步光照数小时,那么完全恢复所需时间会长得多,并且需要新的蛋白质合成。使用分离膜进行的电子传递分析表明,Na⁺耗尽导致的立即抑制涉及放氧位点,而需要新蛋白质合成的次级效应发生在光系统II反应中心附近。在不同pH值和无无机碳的条件下进行的实验表明,在这些实验的短时间内,Na⁺不会通过限制碳酸氢盐进入细胞来抑制光合作用。这些实验扩展了之前对其他蓝细菌的研究结果,这些结果表明Ca²⁺和Na⁺胁迫会在光系统II反应中心附近的位点造成可逆损伤。这种损伤可被表征为在放氧位点的初级离子效应和在光系统II反应中心附近的次级光抑制。