Yoshioka-Nishimura Miho, Yamamoto Yasusi
Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
J Photochem Photobiol B. 2014 Aug;137:100-6. doi: 10.1016/j.jphotobiol.2014.02.012. Epub 2014 Mar 4.
The reaction center-binding D1 protein of Photosystem II is damaged by excessive light, which leads to photoinhibition of Photosystem II. The damaged D1 protein is removed immediately by specific proteases, and a metalloprotease FtsH located in the thylakoid membranes is involved in the proteolytic process. According to recent studies on the distribution and organization of the protein complexes/supercomplexes in the thylakoid membranes, the grana of higher plant chloroplasts are crowded with Photosystem II complexes and light-harvesting complexes. For the repair of the photodamaged D1 protein, the majority of the active hexameric FtsH proteases should be localized in close proximity to the Photosystem II complexes. The unstacking of the grana may increase the area of the grana margin and facilitate easier access of the FtsH proteases to the damaged D1 protein. These results suggest that the structural changes of the thylakoid membranes by light stress increase the mobility of the membrane proteins and support the quality control of Photosystem II.
光系统II的反应中心结合蛋白D1受强光破坏，导致光系统II发生光抑制。受损的D1蛋白会立即被特定蛋白酶清除，位于类囊体膜上的金属蛋白酶FtsH参与了这一蛋白水解过程。根据近期对类囊体膜中蛋白质复合物/超复合物分布和组织的研究，高等植物叶绿体的基粒中挤满了光系统II复合物和捕光复合物。为了修复光损伤的D1蛋白，大多数活性六聚体FtsH蛋白酶应定位在靠近光系统II复合物的位置。基粒的解堆叠可能会增加基粒边缘的面积，并便于FtsH蛋白酶更容易接近受损的D1蛋白。这些结果表明，光胁迫引起的类囊体膜结构变化增加了膜蛋白的流动性，并支持了光系统II的质量控制。
