Identification of factors and genes related to aluminum tolerance acquired during phosphte starvation in tobacco cells.

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Aluminum (Al) is a major factor in the inhibition of plant root growth in acid soils. However, the primary lesion that leads to inhibition of root elongation has not been identified. At cellular level, the stimulatory effect of Al on the Fe (II) -dependent peroxidation of lipids has been reported. In cultured tabacco cells, the peroxidation of lipids caused by Al and Fe (II) together is a primary lesion leading to cell death. Under the condition, tobacco cells starved for phosphate (Pi) exhibit tolerance to the toxicity caused by a combination of Al and Fe (II). In addition, we isolated an Al-tolerant cell line (ALT107) from cultured tobacco cells.In this study, we identified antioxidant molecules related to Al tolerance in Pi-starved cells and ALT107 cells as follows :1. Pi-starved cells accumulated carotenoid pigments (especially beta -carotene). In addition, Pi-starved cells, as well as ALT107 cells, accumulated phenylpropanoids including some derivatives of caffeic acid. The phyenylpropanoid compounds protected tobacco cells from the peroxidation of lipids and cell death caused by Al and Fe (II) together, indicating that the phenylpropanoids have antioxidant activity to interfere with the peroxidation of lipids.2. Pi-starved cells and ALT107 cells exhibited an increase in specific activity of phenylalanine ammonia lyase (PAL). Furthermore, a specific inhibitor of PAL completely brocked the accumulation of the phenylpropanoids in Pi-starved cells and ALT107 cells, indicating that PAL is a key enzyme for the accumulation of the phenylpropanoids in cells.These results suggest that the reguglation of the PAL activity is one of the possible mechanism for tolerance to Al toxicity, especially the toxicity caused by Al-enhanced Fe-mediated peroxidation of lipids.