Ohnishi Norikazu, Allakhverdiev Suleyman I, Takahashi Shunichi, Higashi Shoichi, Watanabe Masakatsu, Nishiyama Yoshitaka, Murata Norio
Division of Cellular Regulation, National Institute for Basic Biology, Okazaki 444-8585, Japan.
Biochemistry. 2005 Jun 14;44(23):8494-9. doi: 10.1021/bi047518q.
Under strong light, photosystem II (PSII) of oxygenic photosynthetic organisms is inactivated, and this phenomenon is called photoinhibition. In a widely accepted model, photoinhibition is induced by excess light energy, which is absorbed by chlorophyll but not utilized in photosynthesis. Using monochromatic light from the Okazaki Large Spectrograph and thylakoid membranes from Thermosynechococcus elongatus, we observed that UV and blue light inactivated the oxygen-evolving complex much faster than the photochemical reaction center of PSII. These observations suggested that the light-induced damage was associated with a UV- and blue light-absorbing center in the oxygen-evolving complex of PSII. The action spectrum of the primary event in photodamage to PSII revealed the strong effects of UV and blue light and differed considerably from the absorption spectra of chlorophyll and thylakoid membranes. By contrast to the photoinduced inactivation of the oxygen-evolving complex in untreated thylakoid membranes, red light efficiently induced inactivation of the PSII reaction center in Tris-treated thylakoid membranes, and the action spectrum resembled the absorption spectrum of chlorophyll. Our observations suggest that photodamage to PSII occurs in two steps. Step 1 is the light-induced inactivation of the oxygen-evolving complex. Step 2, occurring after step 1 is complete, is the inactivation of the PSII reaction center by light absorbed by chlorophyll. We confirmed our model by illumination of untreated thylakoid membranes with blue and UV light, which inactivated the oxygen-evolving complex, and then with red light, which inactivated the photochemical reaction center.
在强光下,产氧光合生物的光系统II(PSII)会失活,这种现象被称为光抑制。在一个被广泛接受的模型中,光抑制是由过量的光能诱导的,这些光能被叶绿素吸收但未用于光合作用。利用冈崎大型光谱仪的单色光和嗜热栖热菌的类囊体膜,我们观察到紫外线和蓝光使放氧复合体失活的速度比PSII的光化学反应中心快得多。这些观察结果表明,光诱导损伤与PSII放氧复合体中一个吸收紫外线和蓝光的中心有关。PSII光损伤初级事件的作用光谱显示了紫外线和蓝光的强烈影响,并且与叶绿素和类囊体膜的吸收光谱有很大差异。与未处理的类囊体膜中放氧复合体的光诱导失活相反,红光能有效地诱导经Tris处理的类囊体膜中PSII反应中心的失活,并且其作用光谱类似于叶绿素的吸收光谱。我们的观察结果表明,PSII的光损伤分两步发生。第一步是光诱导放氧复合体失活。第二步,在第一步完成后发生,是叶绿素吸收的光使PSII反应中心失活。我们通过用蓝光和紫外线照射未处理的类囊体膜来证实我们的模型,蓝光和紫外线使放氧复合体失活,然后用红光照射,红光使光化学反应中心失活。