Plants, Photosynthesis and Soil, School of Biosciences, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK.
Department of Chemical and Biological Engineering, University of Sheffield, Sheffield S1 4NL, UK.
Plant Physiol. 2023 May 2;192(1):370-386. doi: 10.1093/plphys/kiad084.
The light reactions of photosynthesis couple electron and proton transfers across the thylakoid membrane, generating NADPH, and proton motive force (pmf) that powers the endergonic synthesis of ATP by ATP synthase. ATP and NADPH are required for CO2 fixation into carbohydrates by the Calvin-Benson-Bassham cycle. The dominant ΔpH component of the pmf also plays a photoprotective role in regulating photosystem II light harvesting efficiency through nonphotochemical quenching (NPQ) and photosynthetic control via electron transfer from cytochrome b6f (cytb6f) to photosystem I. ΔpH can be adjusted by increasing the proton influx into the thylakoid lumen via upregulation of cyclic electron transfer (CET) or decreasing proton efflux via downregulation of ATP synthase conductivity (gH+). The interplay and relative contributions of these two elements of ΔpH control to photoprotection are not well understood. Here, we showed that an Arabidopsis (Arabidopsis thaliana) ATP synthase mutant hunger for oxygen in photosynthetic transfer reaction 2 (hope2) with 40% higher proton efflux has supercharged CET. Double crosses of hope2 with the CET-deficient proton gradient regulation 5 and ndh-like photosynthetic complex I lines revealed that PROTON GRADIENT REGULATION 5 (PGR5)-dependent CET is the major pathway contributing to higher proton influx. PGR5-dependent CET allowed hope2 to maintain wild-type levels of ΔpH, CO2 fixation and NPQ, however photosynthetic control remained absent and PSI was prone to photoinhibition. Therefore, high CET in the absence of ATP synthase regulation is insufficient for PSI photoprotection.
光合作用的光反应将电子和质子转移穿过类囊体膜，生成 NADPH 和质子动力势（pmf），pmf 为 ATP 合酶将 ATP 合成的吸能反应提供动力。ATP 和 NADPH 是卡尔文-本森-巴斯汉姆循环将 CO2 固定为碳水化合物所必需的。pmf 的主要 ΔpH 成分也通过非光化学猝灭（NPQ）和通过细胞色素 b6f（cytb6f）到光系统 I 的电子转移对光合系统 II 光捕获效率进行光保护调节。通过上调环式电子传递（CET）增加质子流入类囊体腔或通过下调 ATP 合酶电导（gH+）减少质子外排，可以调节 ΔpH。这两个调节 ΔpH 的元素相互作用和相对贡献对光保护的作用尚不清楚。在这里，我们表明，拟南芥（Arabidopsis thaliana）ATP 合酶突变体饥饿在光合转移反应 2（hope2）中，质子外排率高出 40%，CET 被超激化。hope2 与 CET 缺陷型质子梯度调节 5 和 ndh 样光系统 I 复合物的双交叉表明，PGR5 依赖性 CET 是导致质子流入增加的主要途径。PGR5 依赖性 CET 使 hope2 能够维持野生型水平的 ΔpH、CO2 固定和 NPQ，然而光合作用控制仍然不存在，PSI 容易受到光抑制。因此，缺乏 ATP 合酶调节的高 CET 不足以保护 PSI 免受光抑制。
