The role of calmodulin on Al toxicity was studied in two maize (Zea mays L.
) inbred lines, Cat 100-6 (Al-tolerant) and S 1587-17 (Al-sensitive). Incre
asing levels of Al induced the release of malate at similar rate by roots o
f both genotypes, while the exudation of citrate, a stronger Al-binding com
pound, was 3.5 times higher in Cat 100-6 seedlings exposed to 16.2 x 10(-6)
Al3+ activity. The calmodulin inhibitor trifluoperazine significantly redu
ced the root growth in both genotypes, mimicking the main effect of Al. How
ever, when Cat 100-6 and S 1587-17 seedlings were challenged with Al in con
junction with trifluoperazine, no further reduction in root growth or any o
ther effect of Al toxicity was observed. The rate of Al-induced citrate exu
dation by both genotypes was not affected by treatment with trifluoperazine
or calmidazolium, another calmodulin inhibitor. The Al3+ interaction with
cytoplasmic CaM was estimated using models for the binding of Al3+ and Mg2 with CaM and physiological concentrations of citrate, CaM, InsP(3), ATP, A
DP, Al3+ and Mg2+. In this simulation, Al3+ associated with citrate and Ins
P(3), but not with CaM. We conclude that calmodulin is not relevant to the
physiological processes leading to the Al tolerance in maize, nor is it a p
rimary target for Al toxicity. (C) 2001 Elsevier Science Ltd. All rights re
served.