Non-photochemical quenching (NPQ) in photosynthetic organisms provides the necessary photoprotection that allows them to cope with largely and quickly varying light intensities. It involves deactivation of excited states mainly at the level of the antenna complexes of photosystem II using still largely unknown molecular mechanisms. In higher plants the main contribution to NPQ is the so-called qE-quenching, which can be switched on and off in a few seconds. This quenching mechanism is affected by the low pH-induced activation of the small membrane protein PsbS which interacts with the major light-harvesting complex of photosystem II (LHCII). We are reporting here on a mechanistic study of the PsbS-induced LHCII quenching using ultrafast time-resolved chlorophyll (Chl) fluorescence. It is shown that the PsbS/LHCII interaction in reconstituted proteoliposomes induces highly effective and specific quenching of the LHCII excitation by a factor ≥ 20 via Chl-Chl charge-transfer (CT) state intermediates which are weakly fluorescent. Their characteristics are very broad fluorescence bands pronouncedly red-shifted from the typical unquenched LHCII fluorescence maximum. The observation of PsbS-induced Chl-Chl CT-state emission from LHCII in the reconstituted proteoliposomes is highly reminiscent of the in vivo quenching situation and also of LHCII quenching in vitro in aggregated LHCII, indicating a similar quenching mechanism in all those situations. The PsbS mutant lacking the two proton sensing Glu residues induced significant, but much smaller, quenching than wild type. Added zeaxanthin had only minor effects on the yield of quenching in the proteoliposomes. Overall our study shows that PsbS co-reconstituted with LHCII in liposomes represents an excellent in vitro model system with characteristics that are reflecting closely the in vivo qE-quenching situation.

中文翻译：

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关于PsbS诱导的植物脂质体中主要的光捕获复合物LHCII的淬灭。

光合生物中的非光化学猝灭（NPQ）提供了必要的光保护作用，使它们能够应对变化很大且快速变化的光强度。它涉及使用仍然很大程度上未知的分子机制，主要在光系统II的天线复合体水平上使激发态失活。在高等工厂中，对NPQ的主要贡献是所谓的qE猝灭，它可以在几秒钟内打开和关闭。这种猝灭机制受到低pH诱导的小膜蛋白PsbS活化的影响，该蛋白与光系统II（LHCII）的主要光收集复合体相互作用。我们在这里报告有关使用超快时间分辨叶绿素（Chl）荧光的PsbS诱导的LHCII淬灭的机理研究。结果表明，重构的蛋白脂质体中的PsbS / LHCII相互作用通过弱荧光的Chl-Chl电荷转移（CT）状态中间体，以≥20的因子诱导LHCII激发的高效和特异性淬灭。它们的特征是非常宽的荧光带，与典型的非猝灭LHCII荧光最大值相比明显发生了红移。在重组蛋白脂质体中从LHCII观察到PsbS诱导的Chl-Chl CT状态发射非常让人联想到体内淬灭的情况，也很容易让人联想到聚合LHCII在体外的LHCII的淬灭，这表明在所有这些情况下都有类似的淬灭机制。缺少两个质子感应Glu残基的PsbS突变体诱导了显着的但比野生型更小的淬灭。添加的玉米黄质对蛋白脂质体的淬灭产率仅有很小的影响。总体而言，我们的研究表明，脂质体中与LHCII共重构的PsbS代表了一种出色的体外模型系统，其特征与体内qE猝灭情况密切相关。