Roles of ApcD and orange carotenoid protein in photoinduction of electron transport upon dark–light transition in the Synechocystis PCC 6803 mutant deficient in flavodiiron protein Flv1

Abstract

Flavodiiron proteins Flv1/Flv3 accept electrons from photosystem (PS) I. In this work we investigated light adaptation mechanisms of Flv1-deficient mutant of Synechocystis PCC 6803, incapable to form the Flv1/Flv3 heterodimer. First seconds of dark–light transition were studied by parallel measurements of light-induced changes in chlorophyll fluorescence, P700 redox transformations, fluorescence emission at 77 K, and OCP-dependent fluorescence quenching. During the period of Calvin cycle activation upon dark–light transition, the linear electron transport (LET) in wild type is supported by the Flv1/Flv3 heterodimer, whereas in Δflv1 mutant activation of LET upon illumination is preceded by cyclic electron flow that maintains State 2. The State 2–State 1 transition and Orange Carotenoid Protein (OCP)-dependent non-photochemical quenching occur independently of each other, begin in about 10 s after the illumination of the cells and are accompanied by a short-term re-reduction of the PSI reaction center (P700⁺). ApcD is important for the State 2–State 1 transition in the Δflv1 mutant, but S-M rise in chlorophyll fluorescence was not completely inhibited in Δflv1/ΔapcD mutant. LET in Δflv1 mutant starts earlier than the S–M rise in chlorophyll fluorescence, and the oxidation of plastoquinol (PQH₂) pool promotes the activation of PSII, transient re-reduction of P700⁺ and transition to State 1. An attempt to induce state transition in the wild type under high intensity light using methyl viologen, highly oxidizing P700 and PQH₂, was unsuccessful, showing that oxidation of intersystem electron-transport carriers might be insufficient for the induction of State 2–State 1 transition in wild type of Synechocystis under high light.