Minoda Ayumi, Sato Norihiro, Nozaki Hisayoshi, Okada Katsuhiko, Takahashi Haruko, Sonoike Kintake, Tsuzuki Mikio
School of Life Science, Tokyo University of Pharmacy and Life Science, Horinouchi, Hachioji, Japan.
Eur J Biochem. 2002 May;269(9):2353-8. doi: 10.1046/j.1432-1033.2002.02896.x.
The physiological role of sulfoquinovosyl diacylglycerol (SQDG) in photosynthesis was investigated with a SQDG defective mutant (hf-2) of Chlamydomonas reinhardtii that did not have any detectable amount of SQDG. The mutant showed a lower rate of photosystem II (PSII) activity by approximately 40% and also a lower growth rate than those of the wild-type. Results of genetical analysis of hf-2 strongly suggest that the SQDG defect and the lowered PSII activity are due to a single gene mutation. The supplementation of SQDG to hf-2 cells restored the lowered PSII activity to the same level as that of wild-type cells, and also enabled the mutant to grow even in the presence of 135 nm 3-(3,4-dichlorophenyl)-1,1-dimethylurea. Moreover, the incubation of isolated thylakoid membranes of hf-2 with SQDG raised the lowered PSII activity. Chemical modifications of SQDG impaired the recovery of PSII activity. The results suggest that SQDG is indispensable for PSII activity in Chlamydomonas by maintaining PSII complexes in their proper state.
利用莱茵衣藻的硫代奎诺糖基二酰基甘油(SQDG)缺陷型突变体(hf-2)研究了SQDG在光合作用中的生理作用,该突变体中未检测到任何SQDG。该突变体的光系统II(PSII)活性速率比野生型低约40%,生长速率也较低。对hf-2的遗传分析结果强烈表明,SQDG缺陷和PSII活性降低是由单个基因突变引起的。向hf-2细胞补充SQDG可将降低的PSII活性恢复到与野生型细胞相同的水平,并且即使在存在135 nM 3-(3,4-二氯苯基)-1,1-二甲基脲的情况下,该突变体也能够生长。此外,用SQDG孵育hf-2分离的类囊体膜可提高降低的PSII活性。SQDG的化学修饰会损害PSII活性的恢复。结果表明SQDG通过将PSII复合物维持在适当状态,对衣藻中的PSII活性不可或缺。