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

在酸性土壤中，铝离子是限制植物生长的主要因素。我们以前发现，细胞表面的铝离子触发线粒体功能障碍，活性氧（ROS）的产生，并最终导致细胞死亡。本研究的目的是研究铝毒害途径的分子细节，并鉴定与铝耐性相关的分子和/或基因，作为一个重要的早期事件，我们发现铝通过蔗糖-H ^+共转运蛋白抑制烟草细胞的蔗糖吸收。由于铝对蔗糖吸收的抑制和对水分吸收的抑制是同时发生的，因此我们认为铝对蔗糖吸收的抑制导致了对水分吸收的抑制，并最终导致了对细胞伸长的抑制。此外，由于蔗糖摄取的抑制导致线粒体碳源供应减少，这似乎导致线粒体功能障碍和ATP耗竭，最终导致细胞死亡，我们还发现胞浆钙离子浓度的瞬时变化与铝胁迫反应有关的可能性。结果表明，在烟草耐铝细胞中过量表达的过氧化物酶基因为耐铝基因，豌豆根系中ATP含量是决定豌豆耐铝性的因素之一。

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.