Callahan F E, Becker D W, Cheniae G M
University of Kentucky, Lexington, Kentucky 40546.
Plant Physiol. 1986 Sep;82(1):261-9. doi: 10.1104/pp.82.1.261.
Inactivation of the water splitting enzyme complex in leaves or isolated chloroplasts results in increased susceptibility of photosystem II (PSII) to damage by light. Photoinhibition under this condition occurs in very weak light. The site of damage is exclusive of the water splitting complex yet still on the oxidizing side of PSII, as the Q(B) locus is unaffected while photoreduction of silicomolybdate is inhibited. The kinetics of loss in PSII activity are more complex than apparent first-order, and the quantum efficiency is low. We observe no evidence of deletion from thylakoid membranes of any PSII polypeptide as a consequence of photoinhibition, although recovery from the photoinhibition is dependent upon both light and 70S protein synthesis. Enhanced synthesis of two proteins occurs during recovery, only one of which (D2) appears to be causally related to the recovery. We present a model which describes the relationship of weak light photoinhibition and its recovery to photoactivation of the S-state water oxidizing complex.
叶片或分离的叶绿体中水分裂解酶复合物的失活会导致光系统II(PSII)对光损伤的敏感性增加。在这种情况下,光抑制在非常弱的光线下就会发生。损伤部位不包括水分裂解复合物,但仍在PSII的氧化侧,因为Q(B)位点未受影响,而硅钼酸盐的光还原受到抑制。PSII活性丧失的动力学比明显的一级动力学更复杂,且量子效率较低。我们没有观察到光抑制导致任何PSII多肽从类囊体膜上缺失的证据,尽管从光抑制中恢复依赖于光和70S蛋白质合成。恢复过程中会增强两种蛋白质的合成,其中只有一种(D2)似乎与恢复有因果关系。我们提出了一个模型,该模型描述了弱光光抑制及其恢复与S态水氧化复合物的光激活之间的关系。