Probing the role of calmodulin in Al toxicity in maize.
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). Increasing levels of Al induced the release of malate at similar rate by roots of both genotypes, while the exudation of citrate, a stronger Al-binding compound, was 3.5 times higher in Cat 100-6 seedlings exposed to 16.2x10(-6) Al(3+) activity. The calmodulin inhibitor trifluoperazine significantly reduced the root growth in both genotypes, mimicking the main effect of Al. However, when Cat 100-6 and S 1587-17 seedlings were challenged with Al in conjunction with trifluoperazine, no further reduction in root growth or any other effect of Al toxicity was observed. The rate of Al-induced citrate exudation by both genotypes was not affected by treatment with trifluoperazine or calmidazolium, another calmodulin inhibitor. The Al(3+) interaction with cytoplasmic CaM was estimated using models for the binding of Al(3+) and Mg(2+) with CaM and physiological concentrations of citrate, CaM, InsP(3), ATP, ADP, Al(3+) and Mg(2+). In this simulation, Al(3+) associated with citrate and InsP(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 primary target for Al toxicity.
Jorge
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Universidade Estadual de Campinas, UNICAMP, Instituto de Química, Departamento de Físico-Química, SP, Campinas, Brazil. rjorge@iqm.unicamp.br
Menossi
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Arruda
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D000222:Adaptation, Physiological / Q000235:genetics; D000535:Aluminum / Q000378:metabolism / Q000633:toxicity*; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology*; D005838:Genotype; D011485:Protein Binding; D003313:Zea mays / Q000187:drug effects* / Q000235:genetics / Q000502:physiology
D002147:Calmodulin; D000535:Aluminum