Department of Plant Physiology, University of Umeå, S-901 87, Umeå, Sweden.
Photosynth Res. 1993 Feb;35(2):191-200. doi: 10.1007/BF00014750.
Photoinhibition of photosynthesis was studied in intact barley leaves at 5 and 20°C, to reveal if Photosystem II becomes predisposed to photoinhibition at low temperature by 1) creation of excessive excitation of Photosystem II or, 2) inhibition of the repair process of Photosystem II. The light and temperature dependence of the reduction state of QA was measured by modulated fluorescence. Photon flux densities giving 60% of QA in a reduced state at steady-state photosynthesis (300 μmol m(-2)s(-1) at 5°C and 1200 μmol m(-2)s(-1) at 20°C) resulted in a depression of the photochemical efficiency of Photosystem II (Fv/Fm) at both 5 and 20°C. Inhibition of Fv/Fm occurred with initially similar kinetics at the two temperatures. After 6h, Fv/Fm was inhibited by 30% and had reached steady-state at 20°C. However, at 5°C, Fv/Fm continued to decrease and after 10h, Fv/Fm was depressed to 55% of control. The light response of the reduction state of QA did not change during photoinhibition at 20°C, whereas after photoinhibition at 5°C, the proportion of closed reaction centres at a given photon flux density was 10-20% lower than before photoinhibition.Changes in the D1-content were measured by immunoblotting and by the atrazine binding capacity during photoinhibition at high and low temperatures, with and without the addition of chloramphenicol to block chloroplast encoded protein synthesis. At 20°C, there was a close correlation between the amount of D1-protein and the photochemical efficiency of photosystem II, both in the presence or in the absence of an active repair cycle. At 5°C, an accumulation of inactive reaction centres occurred, since the photochemical efficiency of Photosystem II was much more depressed than the loss of D1-protein. Furthermore, at 5°C the repair cycle was largely inhibited as concluded from the finding that blockage of chloroplast encoded protein synthesis did not enhance the susceptibility to photoinhibition at 5°C.It is concluded that, the kinetics of the initial decrease of Fv/Fm was determined by the reduction state of the primary electron acceptor QA, at both temperatures. However, the further suppression of Fv/Fm at 5°C after several hours of photoinhibition implies that the inhibited repair cycle started to have an effect in determining the photochemical efficiency of Photosystem II.
在 5°C 和 20°C 下，通过研究完整大麦叶片中的光合作用光抑制，揭示了 1）是否通过产生过多的 PSII 激发或 2）PSII 修复过程的抑制，PSII 在低温下变得易于光抑制。通过调制荧光测量 QA 的还原态的光和温度依赖性。在稳态光合作用下（5°C 时为 300 μmol m(-2)s(-1)，20°C 时为 1200 μmol m(-2)s(-1)），使 QA 处于还原态的光量子通量密度达到 60%，导致 PSII 的光化学效率（Fv/Fm）在两种温度下均降低。在两种温度下，Fv/Fm 的抑制具有相似的初始动力学。6 小时后，Fv/Fm 被抑制了 30%，并在 20°C 下达到稳定状态。然而，在 5°C 时，Fv/Fm 继续下降，10 小时后，Fv/Fm 被抑制至对照的 55%。在 20°C 下，光抑制过程中 QA 的还原态光响应没有变化，而在 5°C 下光抑制后，给定光量子通量密度下的关闭反应中心的比例比光抑制前低 10-20%。通过免疫印迹和在高、低温下有无添加氯霉素以阻断叶绿体编码蛋白合成的情况下，通过草丁膦结合能力来测量 D1-含量的变化。在 20°C 下，在有或没有活跃的修复循环的情况下，D1-蛋白的量与 PSII 的光化学效率之间存在密切的相关性。在 5°C 时，由于 PSII 的光化学效率比 D1-蛋白的损失更为严重，因此发生了无活性反应中心的积累。此外，由于发现阻断叶绿体编码蛋白合成并不能增强 5°C 下的光抑制敏感性，因此可以得出结论，修复循环在很大程度上受到抑制。在 5°C 下，光抑制几小时后 Fv/Fm 的进一步抑制意味着受抑制的修复循环开始对 PSII 的光化学效率产生影响。综上所述，在两种温度下，Fv/Fm 的初始降低动力学都由最初的电子受体 QA 的还原状态决定。然而，在光抑制数小时后，Fv/Fm 在 5°C 下的进一步抑制意味着受抑制的修复循环开始对 PSII 的光化学效率产生影响。
