Takahashi Shunichi, Murata Norio
National Institute for Basic Biology, Myodaiji, Okazaki 444-8585, Japan.
Biochim Biophys Acta. 2006 Mar;1757(3):198-205. doi: 10.1016/j.bbabio.2006.02.002. Epub 2006 Mar 3.
We demonstrated recently that, in intact cells of Chlamydomonas reinhardtii, interruption of CO2 fixation via the Calvin cycle inhibits the synthesis of proteins in photosystem II (PSII), in particular, synthesis of the D1 protein, during the repair of PSII after photodamage. In the present study, we investigated the mechanism responsible for this phenomenon using intact chloroplasts isolated from spinach leaves. When CO2 fixation was inhibited by exogenous glycolaldehyde, which inhibits the phosphoribulokinase that synthesizes ribulose-1,5-bisphosphate, the synthesis de novo of the D1 protein was inhibited. However, when glycerate-3-phosphate (3-PGA), which is a product of CO2 fixation in the Calvin cycle, was supplied exogenously, the inhibitory effect of glycolaldehyde was abolished. A reduced supply of CO2 also suppressed the synthesis of the D1 protein, and this inhibitory effect was also abolished by exogenous 3-PGA. These findings suggest that the supply of 3-PGA, generated by CO2 fixation, is important for the synthesis of the D1 Protein. It is likely that 3-PGA accepts electrons from NADPH and decreases the level of reactive oxygen species, which inhibit the synthesis of proteins, such as the D1 protein.
我们最近证明,在莱茵衣藻的完整细胞中,通过卡尔文循环固定二氧化碳的过程被中断时,在光损伤后光系统II(PSII)的修复过程中,会抑制PSII中蛋白质的合成,特别是D1蛋白的合成。在本研究中,我们使用从菠菜叶片中分离出的完整叶绿体,研究了导致这种现象的机制。当通过外源性乙醇醛抑制二氧化碳固定时,乙醇醛会抑制合成核酮糖-1,5-二磷酸的磷酸核酮糖激酶,D1蛋白的从头合成受到抑制。然而,当外源性供应卡尔文循环中二氧化碳固定的产物3-磷酸甘油酸(3-PGA)时,乙醇醛的抑制作用就会被消除。二氧化碳供应减少也会抑制D1蛋白的合成,而外源性3-PGA也消除了这种抑制作用。这些发现表明,由二氧化碳固定产生的3-PGA的供应对D1蛋白的合成很重要。3-PGA可能从NADPH接受电子,并降低活性氧的水平,活性氧会抑制诸如D1蛋白等蛋白质的合成。