Molecular mechanisms of the response of photosynthesis to oxidative stress

光系统II的光抑制是由于光系统II的光损伤速率和受损的光系统II修复速率之间的不平衡造成的。光损伤是由光对放氧复合体的直接作用引起的，因此，光损伤对PSII是不可避免的。对氧化胁迫对光损伤和随后修复的影响的研究表明，活性氧主要通过抑制光损伤的修复而不是直接损伤PSII来发挥作用。因此，强光对PSII具有双重作用；它直接损伤PSII，并通过产生ROS抑制PSII的修复。对ROS诱导的修复抑制的研究表明，ROS抑制PSII修复所需的蛋白质的从头合成，如D1蛋白。此外，对多聚体的分析已经确定，ROS抑制的一个主要目标是翻译的延伸步骤。使用蓝藻体外翻译系统的研究表明，在翻译机制中，延伸因子G可能是ROS抑制的主要靶点。在这里，我们提出了一个新的范例，以研究ROS在光抑制中的分子作用。

Ph00otoinhibition of photosystem II (PSII) is due to the imbalance between the rate of photodamage to PSII and the rate of the repair of damaged PSII. Photodamage is initiated by the direct effects of light on the oxygen-evolving complex and, thus, photodamage to PSII is unavoidable. Studies of the effects of oxidative stress on photodamage and subsequent repair have revealed that reactive oxygen species (ROS) act primarily by inhibiting the repair of photodamaged PSII and not by damaging PSII directly. Thus, strong light has dual effects on PSII ; it damages PSII directly and it inhibits the repair of PSII via production of ROS. Investigations of the ROS-induced inhibition of repair have demonstrated that ROS suppress the synthesis de novo of proteins that are required for the repair of PSII, such as the D1 protein. Moreover, analysis of polysomes has determined that a primary target for inhibition by ROS is the elongation step of translation. Investigations using a cyanobacterial translation system in vitro have revealed that elongation factor G might be the primary target, within the translational machinery, of inhibition by ROS. Here we present a new paradigm for the molecular action of ROS in photoinhibition.