Allakhverdiev Suleyman I, Nishiyama Yoshitaka, Miyairi Sachio, Yamamoto Hiroshi, Inagaki Noritoshi, Kanesaki Yu, Murata Norio
Department of Regulation Biology, National Institute for Basic Biology, Myodaiji, Okazaki 444-8585, Japan.
Plant Physiol. 2002 Nov;130(3):1443-53. doi: 10.1104/pp.011114.
Light stress and salt stress are major environmental factors that limit the efficiency of photosynthesis. However, we have found that the effects of light and salt stress on photosystem II (PSII) in the cyanobacterium Synechocystis sp. PCC 6803 are completely different. Strong light induced photodamage to PSII, whereas salt stress inhibited the repair of the photodamaged PSII and did not accelerate damage to PSII directly. The combination of light and salt stress appeared to inactivate PSII very rapidly as a consequence of their synergistic effects. Radioactive labeling of cells revealed that salt stress inhibited the synthesis of proteins de novo and, in particular, the synthesis of the D1 protein. Northern- and western-blotting analyses demonstrated that salt stress inhibited the transcription and the translation of psbA genes, which encode D1 protein. DNA microarray analysis indicated that the light-induced expression of various genes was suppressed by salt stress. Thus, our results suggest that salt stress inhibits the repair of PSII via suppression of the activities of the transcriptional and translational machinery.
光胁迫和盐胁迫是限制光合作用效率的主要环境因素。然而,我们发现光胁迫和盐胁迫对集胞藻6803(Synechocystis sp. PCC 6803)中光系统II(PSII)的影响完全不同。强光诱导PSII发生光损伤,而盐胁迫抑制光损伤PSII的修复,且不会直接加速PSII的损伤。光胁迫和盐胁迫共同作用似乎会因其协同效应而非常迅速地使PSII失活。对细胞进行放射性标记显示,盐胁迫抑制了从头合成蛋白质,尤其是D1蛋白的合成。Northern印迹和Western印迹分析表明,盐胁迫抑制了编码D1蛋白的psbA基因的转录和翻译。DNA微阵列分析表明,盐胁迫抑制了各种基因的光诱导表达。因此,我们的结果表明,盐胁迫通过抑制转录和翻译机制的活性来抑制PSII的修复。