Abstract

AbstractThe action of low pH treatment (pH 3.6) known to release Ca2+ from the oxygen‐evolving complex in photosystem II (PSII) membranes and to induce Ca2+‐revers‐ible inhibition of electron transport at the acceptor side of PSII in thylakoid membranes (TM) was compared in PSII membranes and TM. The rate of the inactivation of electron transport by low pH was four times higher in TM than in PSII membranes. Ferricyanide accelerated the inactivation of PSII membranes but decreased it in the case of TM. Low pH treatment also greatly modified the fluorescence induction kinetics in both preparations, but significant differences have been found in the fluorescence induction kinetics of treated TM and PSII membranes. Calcium restored the electron transport activity and fluorescence induction kinetics in PSII membranes and TM, whereas diphenylcarbazide restored these functions only in PSII membranes. The reactivation of Ca‐depleted PSII membranes was more effective in the dark, whereas the reactivation of TM required weak light. In the case of PSII membranes subjected to low pH citrate buffer, maximal reactivation was observed at 60 mM Ca2+ but for TM about 10 mM Ca2+ was required and 60 mM fully inhibited electron transport in TM during reactivation. These results indicate that the Ca‐dependent inactivation of the acceptor side of PSII in TM after low pH treatment cannot be explained by the extraction of Ca2+ from the oxygen‐evolving complex. It is rather suggested that the Ca2+ involved in this inhibition is bound to the acceptor side of the photosystem near to the QA‐non‐heme iron binding site and may participate in the binding of a polypeptide of the PSII light antenna complex to the PSII reaction center.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call