Reduction of Photosystem I Reaction Center in DrgA Mutant of the Cyanobacterium Synechocystis sp. PCC 6803 Lacking Soluble NAD(P)H:Quinone Oxidoreductase
Reduction of Photosystem I Reaction Center in DrgA Mutant of the Cyanobacterium Synechocystis sp. PCC 6803 Lacking Soluble NAD(P)H:Quinone Oxidoreductase
复制标题
蓝藻集胞藻 DrgA 突变体中光系统 I 反应中心的减少。
DOI:
10.1023/b:biry.0000026203.23785.43
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发表时间:
2004
期刊:
影响因子:
--
通讯作者:
F. V. Yaminsky
中科院分区:
文献类型:
--
作者:
I. Elanskaya;K. Timofeev;V. G. Grivennikova;G. Kuznetsova;L. N. Davletshina;E. Lukashev;F. V. Yaminsky
Photoautotrophically grown cells of the cyanobacteriumSynechocystissp. PCC 6803 wild type and the Ins2 mutant carrying an insertion in thedrgAgene encoding soluble NAD(P)H:quinone oxidoreductase (NQR) did not differ in the rate of light-induced oxygen evolution and Photosystem I reaction center (P700+) reduction after its oxidation with a white light pulse. In the presence of DCMU, the rate of P700+reduction was lower in mutant cells than in wild type cells. Depletion of respiratory substrates after 24 h dark-starvation caused more potent decrease in the rate of P700+reduction in DrgA mutant cells than in wild type cells. The reduction of P700+by electrons derived from exogenous glucose was slower in photoautotrophically grown DrgA mutant than in wild type cells. The mutation in thedrgAgene did not impair the ability ofSynechocystissp. PCC 6803 cells to oxidize glucose under heterotrophic conditions and did not impair the NDH-1-dependent, rotenone-inhibited electron transfer from NADPH to P700+in thylakoid membranes of the cyanobacterium. Under photoautotrophic growth conditions, NADPH-dehydrogenase activity in DrgA mutant cells was less than 30% from the level observed in wild type cells. The results suggest that NQR, encoded by thedrgAgene, might participate in the regulation of cytoplasmic NADPH oxidation, supplying NADP+for glucose oxidation in the pentose phosphate cycle of cyanobacteria.
影响因子:
4.9
作者:
H. Mi;T. Endo;U. Schreiber;T. Ogawa;K. Asada
通讯作者:
H. Mi;T. Endo;U. Schreiber;T. Ogawa;K. Asada
影响因子:
4.9
作者:
H. Mi;T. Endo;U. Schreiber;T. Ogawa;K. Asada
通讯作者:
H. Mi;T. Endo;U. Schreiber;T. Ogawa;K. Asada