Shochat S, Adir N, Gal A, Inoue Y, Mets L, Ohad I
Department of Biological Chemistry, Hebrew University of Jerusalem, Israel.
Z Naturforsch C J Biosci. 1990 May;45(5):395-401. doi: 10.1515/znc-1990-0514.
The effect of unoccupancy of the QB site by plastoquinone on the photoinactivation of reaction center II in a Cyt b6/f-less mutant of Chlamydomonas reinhardtii, B6, was investigated. In these cells the oxidation of plastoquinol generated by electron flow via RC II to plastoquinone and thus the turnover of PQH2/PQ via the QB site are drastically reduced. Reaction center II of the mutant cells was resistant to photoinactivation relative to the control cells as demonstrated by measurements of light-induced destabilization of S2-QB- charge recombination, rise in intrinsic fluorescence and loss of variable fluorescence. These parameters relate to functions involving the reaction center II D 1 protein. The light-induced degradation of D 1 in the mutant cells was also considerably reduced, with a t1/2 value of 7 h as compared, under similar conditions, to about 1.5 h for the control cells. These results indicate that the photoinactivation of RC II and turnover of the D 1 protein are related and require occupancy of the QB site by PQ and its light-driven reduction.
研究了莱茵衣藻细胞色素b6/f缺失突变体B6中质体醌未占据QB位点对反应中心II光灭活的影响。在这些细胞中，通过RC II到质体醌的电子流产生的质体醌醇的氧化以及因此通过QB位点的PQH2/PQ周转大幅减少。如通过测量光诱导的S2-QB-电荷复合的不稳定、固有荧光的增加和可变荧光的损失所证明的，突变体细胞的反应中心II相对于对照细胞对光灭活具有抗性。这些参数与涉及反应中心II D1蛋白的功能有关。突变体细胞中D1的光诱导降解也显著减少，t1/2值为7小时，而在类似条件下，对照细胞约为1.5小时。这些结果表明，RC II的光灭活和D1蛋白的周转是相关的，并且需要PQ占据QB位点及其光驱动的还原。
