PHENYLGLYOXAL MODIFICATION OF THE PHOTOSYSTEM-II REACTION CENTER

作     者：CSATORDAY, K KUMAR, S WARDEN, JT 

作者机构：RENSSELAER POLYTECH INST DEPT CHEM TROY NY 12180 USA 

出 版 物：《BIOCHIMICA ET BIOPHYSICA ACTA》 (Biochim. Biophys. Acta Bioenerg.)

年 卷 期：1987年第890卷第2期

页      面：224-232页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 07[理学] 

基　　金：NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM026133] Funding Source: NIH RePORTER NIGMS NIH HHS [2R01 GM 26133-05] Funding Source: Medline 

主　　题：Photosystem II ESR Phenylglyoxal P-680 Chl chlorophyll DPIP 2,6-dichlorophenol indophenol Mes 4-morpholinoethanesulfonic acid Hepes 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid D-10 digitonin Photosystem II particles TSF-2 triton Photosystem II particles PS I Photosystem I PS II Photosystem II F i initial fluorescence yield F max maximum fluorescence yield F v variable fluorescence yield P-680 primary electron donor of Photosystem II Q a primary quinone electron acceptor Q b secondary quinone electron acceptor Pheo pheophytin 

摘      要：Time-resolved spectroscopic techniques, including optical flash photolysis and eletron spin resonance (ESR), have been used in conjunction with fluorescence-induction and dye-reduction assays to monitor electron transport in Photosystem II (PS II) subchloroplast particles incubated with the covalent modifier, phenylglyoxal. Phenylglyoxal-modified digitonin (D-10) particles from spinach are characterized by (1) a high initial fluorescence yield (Fi) and an abolition of the variable component of fluorescence (Fv);(2) and inhibition of PS-II-mediated reduction of dichlorophenol indophenol (DPIP) by sym-diphenylcarbazide;(3) an abolition of flash-induced absorption transients (t1/2 2 .mu.s) at 820 nm attributed to the primary electron donor, P-680+;(4) the inhibition of photoreduction of the acceptor Qa;and (5) the elimination of the ESR Signal 2s and Signal 2f. These observations suggest the critical participation of specific arginine residues on both the oxidizing and reducing sides of Photosystem II and also implicate phenylglyoxal as a quinone-binding site inhibitor (Golbeck, J.H. and Warden, J.T. (1984) Biochim. Biophys. Acta 767, 263-271).