D1 fragmentation in photosystem II repair caused by photo-damage of a two-step model
D1 fragmentation in photosystem II repair caused by photo-damage of a two-step model
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DOI：
10.1007/s11120-015-0144-7
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发表时间：
2015-12-01
影响因子：
3.7
通讯作者：
Sakamoto, Wataru
中科院分区：
文献类型：
--
作者：
Kato, Yusuke;Ozawa, Shin-ichiro;Sakamoto, Wataru
光能驱动光合作用，但同时也会使光合作用机制失活。光损伤的主要目标位点是光系统 II (PSII)。它进一步针对一种反应中心蛋白 D1，该蛋白由 PSII 修复周期有效维持。已知两种蛋白酶 FtsH 和 Deg 分别通过持续和内切蛋白水解有效降解光损伤的 D1 蛋白来促进这一过程。本研究测试了这些蛋白酶完成的 D1 裂解是否受到不同单色光（例如蓝色和红色发光二极管光源）的影响，同时注意这些光的使用区分了当前的光抑制模型：过剩能量模型和两步模型。值得注意的是，在两步模型中，主要损伤是由 Mn 团簇吸收光能造成的，蓝色光源而不是红色光源可以增强这种吸收。结果表明，蓝光和红光对 D1 降解的影响不同。一个突出的发现是，在缺乏 FtsH2 的突变体中，蓝光增强了由管腔 Deg 蛋白酶特异性产生的 D1 断裂，但红光则没有增强。尽管是间接证据，但该证据支持 PSII 光损伤的两步模型。我们推断腔内 Deg 蛋白酶增强的 D1 断裂是对 Mn 簇初级损伤的反应。
Light energy drives photosynthesis, but it simultaneously inactivates photosynthetic mechanisms. A major target site of photo-damage is photosystem II (PSII). It further targets one reaction center protein, D1, which is maintained efficiently by the PSII repair cycle. Two proteases, FtsH and Deg, are known to contribute to this process, respectively, by efficient degradation of photo-damaged D1 protein processively and endoproteolytically. This study tested whether the D1 cleavage accomplished by these proteases is affected by different monochromic lights such as blue and red light-emitting-diode light sources, remaining mindful that the use of these lights distinguishes the current models for photoinhibition: the excess-energy model and the two-step model. It is noteworthy that in the two-step model, primary damage results from the absorption of light energy in the Mn-cluster, which can be enhanced by a blue rather than a red light source. Results showed that blue and red lights affect D1 degradation differently. One prominent finding was that D1 fragmentation that is specifically generated by luminal Deg proteases was enhanced by blue light but not by red light in the mutant lacking FtsH2. Although circumstantial, this evidence supports a two-step model of PSII photo-damage. We infer that enhanced D1 fragmentation by luminal Deg proteases is a response to primary damage at the Mn-cluster.