Figure 8.

Schematic Diagram of Electron Transfer Reactions Involved in Oxygenic Photosynthesis in Chloroplasts and Mitochondria and Their Regulation in the Absence of PGRL1-Mediated CEF.

During reactions of linear electron transport, reducing equivalents generated at PSII are sequentially transferred to plastoquinones (PQ/PQH₂), cytochrome (Cyt) b₆/f complex, plastocyanin (Pc), PSI, Fd, and to ferredoxin NADP⁺ reductase (FNR). A pathway of cyclic electron flow around PSI is mediated by PGRL1 and another one by NDA2. In the absence of PGRL1, the deficiency in ATP is compensated for by different mechanisms, sequentially triggered depending on the intensity of the ATP demand. (1) A first compensation mechanism operates via cooperation with mitochondrial respiration, likely involving the oxaloacetate/malate shuttle (or malate valve), which allows export of reducing power from the chloroplast to the cytosol and from the cytosol to mitochondria. In mitochondria, reducing power is converted by the electron transport chain into ATP, which can reenter the chloroplast via ATP translocators. (2) Oxygen photoreduction may occur at the level of NADPH thanks to the action of FLVA and FLVB proteins, which accumulate to higher amounts in pgrl1 and would allow ATP biosynthesis through pseudocyclic photophosphorylation. (3) When mechanisms (1) and (2) are overengaged, the PQ pool becomes more reduced, and the STT7 kinase is activated, thus inducing LHCII phosphorylation and transition from State 1 to State 2 in pgrl1. (4) Finally overreduction of PSI acceptors would trigger true Mehler reactions through direct O₂ photoreduction via reduced Fd, thus producing H₂O₂. (5) Accumulation of ROS would then increase AOX and decrease PSI protein amounts, thus decreasing the PSI/PSII ratio.