Effects of Ca2+ and EGTA on P680·+ reduction kinetics and O2 evolution of Photosystem II

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Abstract

We report for the first time significant changes in the P680·+ reduction kinetics of Photosystem II (PS II) in which the 17 and 23 kDa extrinsic polypeptides are intact, in the presence of Ca2+ or ethylene glycol bis (β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid (EGTA) which were added to vary the Ca2+ concentration from 5 μM to 30 mM. The decrease in the extent of normal P680·+ reduction decay with lifetimes of 40-370 ns and a corresponding increase in the extent of kinetics with lifetimes of 20-220 μs was interpreted as being due to electron transfer from YZ to P680·+ being replaced by slow forward conduction and by processes including P680·+/QA- recombination. The question of whether changes in P680·+ reduction kinetics were caused by loss of Ca2+ from PS II or by direct interaction of EGTA with PS II was addressed by lowering the free-Ca2+ concentration of suspensions of PS II core complexes by serial dilution in the absence of EGTA. Despite a significant decrease in the rate of O2 evolution after this treatment, only small changes in the P680·+ reduction kinetics were observed. Loss of Ca2+ did not affect P680·+ reduction associated with electron transfer from YZ. Since much larger changes in the P680·+ reduction kinetics of intact PS II occurred at comparable free-Ca2+ concentrations in the presence of EGTA, we conclude that EGTA influenced the P680·+ reduction kinetics by directly interacting with PS II rather than by lowering the free Ca2+ concentration of the surrounding media. Notwithstanding these effects, we show that useful information about Ca2+ binding to PS II can be obtained when direct interaction of EGTA is taken into account. © 2003 Elsevier B.V. All rights reserved.

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APA

Stevens, G. B., & Lukins, P. B. (2003). Effects of Ca2+ and EGTA on P680·+ reduction kinetics and O2 evolution of Photosystem II. Biochimica et Biophysica Acta - Bioenergetics, 1605(1–3), 21–34. https://doi.org/10.1016/S0005-2728(03)00061-6

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