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.
