Analyses of aluminum-induced cell death via mitochondrial dysfunction in plant cells.

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In acidic soils, aluminum(Al) ion is a major factor to limit plant growth. We have previously found that Al ion on the cell surface triggers mitochondrial dysfunction, reactive oxygen species(ROS) production and eventually cell death. The purpose of this research was to investigate the molecular details of the Al toxicity pathway, and to identify molecules and/or genes related to Al tolerance.As an important early event, we found that Al inhibits sucrose uptake via sucrose-H^+ cotransporter in cultured tobacco cells. Since the inhibition of sucrose uptake and the inhibition of water uptake were induced simultaneously by Al, we concluded that the Al-induced inhibition of sucrose uptake leads to the inhibition of water uptake and eventually the inhibition of cell elongation. In addition, since the inhibition of sucrose uptake leads to a decrease in the supply of carbon source to mitochondria, which seems to lead to mitochondrial dysfunction and ATP depletion, and finally cell death.We also found a possibility that transient changes of cytosolic calcium ion concentration are related to Al-stress responses. We finally found that the peroxidase gene overexpressed in Al-tolerant tobacco cells is Al-tolerant gene, and that ATP content is one of determining factors of Al tolerance in pea roots.