Overreduction states of photosystem I (PSI) cause PSI photoinhibition. To examine the degree of PSI photoinhibition, changes in its electron transport activity and core-subunit content were evaluated. In contrast, the involvement of peripheral subunits, such as the light-harvesting complex I (LHCI), is less discussed in PSI photoinhibition. Here, we aimed to elucidate whether the light-harvesting functions of LHCI are altered by PSI photoinhibition in rice leaves. To this end, a new method to estimate the functional antenna size of the PSI-LHCI complex was developed using a far-red light-dependent absorption change in the oxidized reaction center chlorophyll (P700 +) in intact leaves, and the obtained kinetics were analyzed using the double Gompertz model. Subsequently, our original parameter, kfast (Far Red-Photon Flux Density) -1, showed a linear response to leaf LHCI content, and the parameter decreased with a decrease in P700 content by PSI photoinhibition in leaves. Furthermore, we found that the susceptibility of LHCI to PSI photoinhibitory treatment decreased with increasing in growth light intensity. Our results suggest that LHCI is a target of PSI photoinhibition, as well as the core-subunits, and rice plants can lower the risk of LHCI photoinhibition through light acclimation responses.

Phosphorus (P) is an essential mineral nutrient for plants. Nevertheless, excessive P accumulation in leaf mesophyll cells causes necrotic symptoms in land plants; this phenomenon is termed P toxicity. However, the detailed mechanisms underlying P toxicity in plants have not yet been elucidated. This study aimed to investigate the molecular mechanism of P toxicity in rice. We found that under excessive inorganic P (Pi) application, Rubisco activation decreased and photosynthesis was inhibited, leading to lipid peroxidation. Although the defence systems against reactive oxygen species (ROS) accumulation were activated under excessive Pi application conditions, the Cu/Zn-type superoxide dismutase activities were inhibited. A metabolic analysis revealed that excessive Pi application led to an increase in the cytosolic sugar phosphate concentration and the activation of phytic acid synthesis. These conditions induced mRNA expression of genes that are activated under metal-deficient conditions, although metals did accumulate. These results suggest that P toxicity is triggered by the attenuation of both photosynthesis and metal availability within cells mediated by phytic acid accumulation. Here, we discuss the whole phenomenon of P toxicity, beginning from the accumulation of Pi within cells to death in land plants.

Phosphorus (P) is one of the essential mineral nutrients for plants. Nevertheless, large amounts of accumulated P easily wither whole plants, and this phenomenon is termed as P toxicity. For improving P-use efficiency, to overcome P toxicity is necessary for plant growth. However, the detailed mechanisms underlying P toxicity in plants have not yet been elucidated. In this study, we aimed to investigate the molecular mechanism of P toxicity in rice. We found that, under excessive inorganic-P (Pi) application conditions, Rubisco activation decreased and photosynthesis was inhibited, leading to lipid-peroxidation. Although the defense systems against reactive oxygen species accumulation were activated under excessive Pi application conditions, the Cu/Zn-type superoxide dismutase activity was inhibited. A metabolic analysis revealed that excess Pi application led to an increase in the cytosolic sugar-phosphate content, and activation of phytic acid synthesis. These conditions induced mRNA expressions of the genes that are activated under metal-deficiency conditions, although metals were rather accumulated. These results suggested that P toxicity is triggered by the attenuation of both photosynthesis, and metal availability within cells mediated by phytic acid accumulation. Here, we discuss the whole phenomenon of P toxicity, beginning from the accumulation of Pi within cells to death in plants.