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.