Photosystem II (PS II) catalyzes the light-driven process of water splitting in oxygenic photosynthesis. Four core membrane-spanning proteins, including D1 that binds the majority of the redox-active co-factors, are surrounded by 13 low-molecular-weight (LMW) proteins. We previously observed that deletion of the LMW PsbT protein in the cyanobacterium Synechocystis sp. PCC 6803 slowed electron transfer between the primary and secondary plastoquinone electron acceptors Q_A and Q_B and increased the susceptibility of PS II to photodamage. Here we show that photodamaged ∆PsbT cells exhibit unimpaired rates of oxygen evolution if electron transport is supported by HCO₃⁻ even though the cells exhibit negligible variable fluorescence. We find that the protein environment in the vicinity of Q_A and Q_B is altered upon removal of PsbT resulting in inhibition of Q_A⁻ oxidation in the presence of 2,5-dimethyl-1,4-benzoquinone, an artificial PS II-specific electron acceptor. Thermoluminescence measurements revealed an increase in charge recombination between the S₂ oxidation state of the water-oxidizing complex and Q_A⁻ by the indirect radiative pathway in ∆PsbT cells and this is accompanied by increased ¹O₂ production. At the protein level, both D1 removal and replacement, as well as PS II biogenesis, were accelerated in the ∆PsbT strain. Our results demonstrate that PsbT plays a key role in optimizing the electron acceptor complex of the acceptor side of PS II and support the view that repair and biogenesis of PS II share an assembly pathway that incorporates both de novo synthesis and recycling of the assembly modules associated with the core membrane-spanning proteins.

光系统II（PS II）在光合作用中催化光分解水的过程。13种低分子量（LMW）蛋白围绕着四个核心跨膜蛋白，其中包括与大多数氧化还原活性辅助因子结合的D1。我们先前观察到的蓝藻Synechocystis sp。中的LMW PsbT蛋白的删除。PCC 6803减缓了主要和次要质体醌电子受体Q _A和Q _B之间的电子转移，并增加了PS II对光损伤的敏感性。在这里，我们表明，光损伤ΔPsbT细胞表现出析氧的速率不受损害，如果电子传输是通过支持HCO ₃ ^-即使细胞表现出微不足道的可变荧光。我们发现，在Q的附近的蛋白质环境_阿和Q_乙是在去除的PSBT从而抑制Q的改变_甲^-氧化2,5-二甲基-1,4-苯醌的存在下，人工PS II-特定电子受体。热释测量显示在S之间在电荷复合的增加₂的氧化状态的水氧化的复杂和Q_甲^-通过在ΔPsbT细胞间接辐射通路，这是伴随着增加¹ Ò ₂生产。在蛋白质水平上，在∆PsbT菌株中，D1的去除和置换以及PS II的生物发生均被加速。我们的结果表明，PsbT在优化PS II受体侧的电子受体复合物方面起着关键作用，并支持以下观点：PS II的修复和生物合成共享一个组装途径，该途径既包括从头合成又包括相关组装模块的回收与核心跨膜蛋白。