Aluminum Induces a Decrease in Cytosolic Calcium Concentration in BY-2 Tobacco Cell Cultures.
David L. Jones, Leon V. Kochian, and Simon Gilroy
School of Agricultural and Forest Sciences, University of Wales, Bangor, Gwynedd LL57 2UW, United Kingdom (D.L.J.), United States Soil and Nutrition Laboratory, United States Department of Agriculture-Agricultural Research Station, Cornell University, Ithaca, New York 14853 (L.V.K.), and Biology Department, Pennsylvania State University, 208 Mueller Building, University Park, Pennsylvania 16802 (S.G.)
Abstract.
Aluminum 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 concentration ([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 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 La3+, but not verapamil or 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.
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