Molecular Basis of the Vulnerability of Photosystem II to Damage by Light

Abstract

Using isolated reaction centres and cores of photosystem I1 (PSII) it has been possible to elucidate the details of two separate pathways which lead to photoinhibition. The acceptor side pathway involves charge recombination resulting in the formation of the triplet state of the primary electron donor, P680. This triplet state is harmless in the absence of oxygen but in its presence gives rise to highly reactive singlet oxygen. We have shown that this singlet oxygen specifically attacks the chlorophyll of P680 itself. This process, plus other possibilities, gives rise to degradation of Dl protein involving a primary cleavage in the stromal loop joining putative transmembrane regions four and five, to yield 23 kDa N-terminal and 10 kDa C-terminal fragments. In contrast a donor side pathway is oxygen independent and is due to detrimental secondary oxidations brought about by P680⁺. Oxidation of accessory chlorophyll (C670) and β-carotene are observed and D1 protein is degraded by a primary cleavage in the lumenal loop between the putative transmembrane segments one and two to yield 24 kDa C-terminal and 9 kDa N-terminal fragments. In vivo studies indicate that the acceptor pathway is more common. The reason for the inherent vulnerability of PSII to photoinduced damage is discussed in terms of the special nature of P68O and the implications of the role of cytochrome b559 as a versatile protectant against donor and acceptor side photoinactivation is also considered. The likely dimeric organisation of PSII in vivo adds an additional factor to the general discussion of the molecular processes which underlie the vulnerability of PSII to photoinduced damage.