The molecular basis of D1 degradation and photosystem two repair

植物的生长对环境中的光线强度极为敏感。在低光强度下，由于没有足够的光来驱动光合作用，生长受到限制。在较高的强度下，由于光对叶绿体中的光合装置的破坏作用，生长受到抑制。这种光抑制现象对作物产量有深远的影响，特别是当植物受到强光和其他胁迫条件（如热胁迫和水分胁迫）的组合时。叶绿体中光损伤的目标之一是参与水氧化和光合电子传递的光系统二复合体，特别是D1蛋白。植物已经发展出一种修复机制，用新合成的拷贝取代受损的D1。在大多数情况下，这种修复机制允许维持PSII活性。然而，在高光强下，修复的速度无法与PSII损伤的速度相匹配，在这些条件下，PSII活性和光合性能都有净损失。原则上，改善修复机制是产生更多耐光植物的途径之一。迄今为止，PSII修复的分子细节尚不清楚，特别是受损D1从膜上移除的过程。最近我们发现了一类特殊的蛋白酶（FtsH蛋白酶），它是D1降解所必需的。我们还发现，在蓝藻中，D1的n端对D1的降解很重要，而蓝藻与叶绿体密切相关。这使我们假设D1降解的机制涉及到FtsH蛋白酶对受损D1的n端的识别。我们的假设与目前科学文献中的模型不一致。在这个建议中，我们设计了一系列的实验来区分这两种模型。最终，这项工作的结果将为植物PSII修复提供一个更清晰的画面。

Plant growth is exquisitely sensitive to the intensity of light in the environment. At low light intensities, growth is limited because of insufficient light to drive photosynthesis. At higher intensities, growth becomes inhibited because of the damaging effects of light on the photosynthetic apparatus found in the chloroplast. This phenomenon of photoinhibition has a profound effect on crop yields especially when plants are subjected to high light in combination with other stress conditions such as heat and water stress. One of the targets of light damage in the chloroplast is the photosystem two complex, which is involved in water oxidation and photosynthetic electron transport, and in particular the D1 protein. Plants have developed a repair mechanism to replace damaged D1 by a newly synthesised copy. Under most conditions this repair mechanism allows PSII activity to be maintained. However at high light intensities the rate of repair is unable to match the rate of damage to PSII and under these conditions there is a net loss of PSII activity and photosynthetic performance. In principle, improving the repair mechanism is one route by which more light-resistant plants can be generated. As yet the molecular details of PSII repair are unclear, especially the process by which damaged D1 is removed from the membrane. Recently we discovered the identity of a particular class of protease (FtsH proteases) that was needed for D1 degradation. We have also discovered that the N-terminus of D1 is important for D1 degradation in cyanobacteria, which are closely related to chloroplasts. This has led us to postulate a mechanism for D1 degradation that involves the recognition of the N-terminus of damaged D1 by the FtsH protease. Our hypothesis is at odds with the current model in the scientific literature. In this proposal we have designed a series of experiments to differentiate between the two models. Ultimately the results of this work will provide a clearer picture of PSII repair in plants.