Calcium-aluminium interactions in the cell wall and plasma membrane of Chara

• Published in: Planta Vol. 195; no. 3; pp. 362 - 368
• Main Authors: Reid, R.J, Tester, M.A, Smith, F.A
• Format: Journal Article
• Language: English
• Published: 1995
• Subjects: aluminum; calcium; cations; cell wall components; cell walls; Chara; electrophysiology; growth; inhibition; inorganic ions; ion activity; ion transport; lanthanum; phytotoxicity; plasma membrane; potassium; rubidium; sodium; vacuoles
• ISSN: 0032-0935; 1432-2048
• DOI: 10.1007/BF00202593

The proposal that aluminium (Al) toxicity in plants is caused by either inhibition of Ca2+ influx or by displacement of Ca2+ from the cell wall, was examined. For this study the giant alga Chara corallina Klein ex Will. em. R.D. Wood was selected because it shows a similar sensitivity to Al as in roots of higher plants and, more importantly, it is possible to use the large single internodal cells to make accurate and unambiguous measurements of Ca2+ influx and Ca2+ binding in cell walls. Growth of Chara was inhibited by Al at concentrations comparable to those required to inhibit growth of roots, and with a similar speed of onset and pH dependence. At Al concentrations which inhibited growth, influx of calcium (Ca2+) was only slightly sensitive to Al. The maximum inhibition of Ca2+ influx at 0.1 mol.m-3 Al at pH 4.4 was less than 50%. At the same concentration, lanthanum (La3+) inhibited influx of Ca2+ by 90% but inhibition of growth was similar for both La3+ and Al. Removal of Ca2+ from the external solution did not inhibit growth for more than 8 h whereas inhibition of growth by Al was apparent after only 2.5 h. Ca2+ influx was more sensitive to Al when stimulated by addition of high concentrations of potassium (K+) or by action potentials generated by electrical stimulation. Other membrane-related activities such as sodium influx, rubidium influx and membrane potential difference and conductance, were not strongly affected by Al even at high concentrations. In isolated cell walls equilibrated in 0.5 mol.m-3 Ca2+ at pH 4.4, 0.1 mol.m-3 Al displaced more than 80% of the bound Ca2+ with a half-time of 25 min. From the poor correlation between inhibition of growth and reduction in Ca2+ influx, it was concluded that Al toxicity was not caused by limitation of the Ca2+ supply. Short-term changes in other membrane-related activities induced by Al also appeared to be too small to explain the toxicity. However the strong displacement, and probable replacement, of cell wall Ca2+ by Al may be sufficient to disrupt normal cell development.