Unifying model for the photoinactivation of Photosystem II in vivo under steady-state photosynthesis
Unifying model for the photoinactivation of Photosystem II in vivo under steady-state photosynthesis
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DOI：
10.1023/a:1005946808488
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发表时间：
1998-04-01
影响因子：
3.7
通讯作者：
Soon, WS
中科院分区：
文献类型：
--
作者：
Anderson, JM;Park, YI;Soon, WS
我们基于目前体内研究的观察结果，而不是分离的类囊体或 PS II 膜的体外研究，提出了一种统一的光抑制机制。体外研究与体内光抑制的相关性有限，因为在自然界中很少遇到的光子暴露中使用非常强的光，并且活细胞中 PS II 调节的大多数多重相互作用的保护策略不起作用。现在已经确定，体内光系统 II 的光失活是一种概率和光剂量事件，取决于吸收的光子而不是每皮下的辐照度。由于遵循互易律并且目标理论分析强烈表明只需要一个光子，因此我们提出在有限、饱和或持续高光下，一个光子在体内发生单一主导分子机制，使 PS II 失活。已经提出了两种高光下光抑制机制，即受体侧和供体侧光抑制[参见 Aro 等人，2017]。 (1994) Biochim Biophys Acta 1143: 113-134]，以及极弱光的另一种机制，即弱光综合症 [Keren 等人。 （1995）生物化学杂志 270：806-814]。基于激子动力学的激子-自由基对平衡模型，我们提出了稳态光合作用下PS II体内光失活的统一机制，该机制取决于主要自由基对P680(+)Pheo(-)浓度增加的产生和维持，以及在不同环境条件下调节电荷重组的不同方式[Anderson等人，2017]。 （1997）生理学植物 100：214-223]。我们认为 D1 蛋白受损的主要原因是 P680(+)，而不是单线态 O-2。由三线态 P680 或其他活性氧形成。
We present a unifying mechanism for photoinhibition based on current obsevations from in vivo studies rather than from in vitro studies with isolated thylakoids or PS II membranes. In vitro studies have limited relevance for in vivo photoinhibition because very high light is used with photon exposures rarely encountered in nature, and most of the multiple, interacting, protective strategies of PS II regulation in living cells are not functional. It is now established that the photoinactivation of Photosystem II in vivo is a probability and light-dosage event which depends on the photons absorbed and not the irradiance per sc. As the reciprocity law is obeyed and target theory analysis strongly suggests that only one photon is required, we propose that a single dominant molecular mechanism occurs in vivo with one photon inactivating PS II under limiting, saturating or sustained high light. Two mechanisms have been proposed for photoinhibition under high light, acceptor-side and donor-side photoinhibition [see Aro et al. (1994) Biochim Biophys Acta 1143: 113-134], and another mechanism for very low light, the low-light syndrome [Keren et al. (1995) J Biol Chem 270: 806-814]. Based on the exciton-radical pair equilibrium model of exciton dynamics, we propose a unifying mechanism for the photoinactivation of PS II in vivo under steady-state photosynthesis that depends on the generation and maintenance of increased concentrations of the primary radical pair, P680(+)Pheo(-), and the different ways charge recombination is regulated under varying environmental conditions [Anderson et al. (1997) Physiol Plant 100: 214-223]. We suggest that the primary cause of damage to D1 protein is P680(+), rather than singlet O-2. formed from triplet P680, or other reactive oxygen species.