Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/22/1998
Publication Date: N/A
Interpretive Summary: Large areas of land within the U.S. and over 40% of the world's arable lands are acidic. In these acid soils, the phytotoxic aluminum (Al) ion, Al3+, is solubilized into soil solution and is toxic to root growth and function. Thus, Al toxicity is the primary factor limiting crop production on these acid soils. Understanding the cellular basis of aluminum toxicity is important in developing crop species that can tolerate Al toxicity and be cultivated on these acid soils. In this paper, we tested a hypothesis that has been frequently suggested in the literature that Al toxicity involves Al-induced disruption of the regulation of the concentration of free calcium ion in the cell. All living cells regulate their free calcium ion concentrations at very low levels, and rapid increases in cell calcium concentration are used as a cellular switch to control many processes. If this regulation is disrupted, cell death or impaired cell development results. In this study, we looked at the effect of Al exposure on cellular calcium concentrations in tobacco cells growing in solution. These cells grow in a manner similar to growing cells within a root. Al exposure rapidly inhibited tobacco cell growth, and also caused a dramatic drop in cellular Ca levels. The Al-induced drop in cellular Ca preceded the onset of Al toxicity (inhibited cell growth) and could have played an important role in toxicity. It appears that external Al blocks the movement of Ca into the growing tobacco cells and this blockage likely plays an important role in the mechanism of Al toxicity.
Technical Abstract: Aluminum (Al) toxicity is a major problem limiting crop productivity on acid soils. It has been suggested that Al toxicity is linked to changes in cellular calcium homeostasis and the blockage of plasma membrane Ca2+- permeable channels. BY-2 suspension culture cells of tobacco exhibit rapid cell expansion that is sensitive to Al. Therefore, the effect of Al on changes in cytoplasmic free calcium activity ([Ca2+]cyt) was followed in BY-2 cells to assess whether Al perturbed cellular calcium homeostasis. Al exposure resulted in a prolonged reduction in [Ca2+]cyt and inhibition of growth that was similar to the effect of the Ca2+ channel blocker La3+ and the Ca2+ chelator EGTA. The organic Ca2+ channel blockers verapamil and nifedipine did not induce a decrease in [Ca2+]cyt in these cells and also failed to inhibit growth. Al and La, but not verapamil and nifedipine reduced the rate of Mn2+ quenching of Indo-1 fluorescence, consistent with the blockage of Ca2+ and Mn2+ permeable channels. These results suggest that Al may act to block Ca2+ channels at the plasma membrane of plant cells and this action may play a crucial role in the phytotoxic activity of the aluminum ion.