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Early events responsible for aluminum toxicity symptoms in suspension‐cultured tobacco cells
Author(s) -
Sivaguru Mayandi,
Yamamoto Yoko,
Rengel Zdenko,
Ahn Sung Ju,
Matsumoto Hideaki
Publication year - 2005
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.2004.01219.x
Subject(s) - callose , depolarization , nicotiana tabacum , intracellular , calcium in biology , calcium , cyclopiazonic acid , biophysics , membrane potential , chemistry , biology , biochemistry , cell wall , organic chemistry , gene
Summary• We investigated the aluminum (Al)‐induced alterations in zeta potential, plasma membrane (PM) potential and intracellular calcium levels to elucidate their interaction with callose production induced by Al toxicity. • A noninvasive confocal laser microscopy has been used to analyse the live tobacco ( Nicotiana tabacum ) cell events by means of fluorescent probes Fluo‐3 acetoxymethyl ester (intracellular calcium) and DiBAC 4 (PM potential) as well as to monitor callose accumulation. • Log‐phase cells showed no detectable changes in the PM potential during the first 30 min of Al treatment, but sustained large depolarization from 60 min onwards. Measurement of zeta potential confirmed the depolarization effect of Al, but the kinetics were different. The Al‐treated cells showed a moderate increase in intracellular Ca 2+ levels and callose production in 1 h, which coincided with the time course of PM depolarization. Compared with the Al treatment, cyclopiazonic acid, an inhibitor of endoplasmic reticulum Ca 2+ ‐ATPase, facilitated a higher increase in intracellular Ca 2+ levels, but resulted in accumulation of only moderate levels of callose. Calcium channel modulators and Al induced similar levels of callose in the initial 1 h of treatment. • Callose production induced by Al toxicity is dependent on both depolarization of the PM and an increase in intracellular Ca 2+ levels.