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|標題:||Identification and characterization of a cytochrome b559 Synechocystis 6803 mutant spontaneously generated from DCMU-inhibited photoheterotrophical growth conditions||作者:||Chiu, Y.F.
|關鍵字:||Photosystem II;Cytochrome b559;Photoinhibition;Chlorophyll a;fluorescence;Site-directed mutagenesis;Synechocystis;EPR;synechocystis sp pcc-6803;cyanobacterial photosystem-ii;singlet oxygen;production;redox properties;directed mutagenesis;spectral properties;manganese cluster;potential form;higher-plants;b(559)||Project:||Biochimica Et Biophysica Acta-Bioenergetics||期刊/報告no：:||Biochimica Et Biophysica Acta-Bioenergetics, Volume 1787, Issue 10, Page(s) 1179-1188.||摘要:||
We identified a spontaneously generated mutant from Synechocystis sp. PCC6803 wild-type cells grown in BG-11 agar plates containing 5 mM Glu and 10 mu M DCMU. This mutant carries an R7L mutation on the alpha-subunit of cyt b559 in photosystem II (PSII). In the recent 2.9 angstrom PSII crystal structural model, the side chain of this arginine residue is in close contact with the heme propionates of cyt b559. We called this mutant WR7L alpha cyt b559. This mutant grew at about the same rate as wild-type cells under photoautotrophical conditions but grew faster than wild-type cells under photoheterotrophical conditions. In addition, 77 K fluorescence and 295 K chlorophyll a fluorescence spectral results indicated that the energy delivery from phycobilisomes to PSII reaction centers was partially inhibited or uncoupled in this mutant. Moreover, WR7L alpha cyt b559 mutant cells were more susceptible to photoinhibition than wild-type cells under high light conditions. Furthermore, our EPR results indicated that in a significant fraction of mutant reaction centers, the R7L alpha cyt 15559 mutation induced the displacement of one of the axial histidine ligands to the heme of cyt b559. On the basis of these results, we propose that the Arg7Leu mutation on the alpha-subunit of cyt 15559 alters the interaction between the APC core complex and PSII reaction centers, which reduces energy delivery from the antenna to the reaction center and thus protects mutant cells from DCMU-induced photo-oxidative stress. (C) 2009 Elsevier B.V. All rights reserved.
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