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pubmed:abstractText |
A variety of plant species emit volatile compounds in response to mechanical stresses such as herbivore attack. Although these volatile compounds promote gene expression leading to anti-herbivore responses, the underlying transduction mechanisms are largely unknown. While indirect evidence suggests that the cytoplasmic free Ca(2+) concentration ([Ca(2+)](c)) plays a crucial role in the volatile-sensing mechanisms in plants, these roles have not been directly demonstrated. In the present study, we used Arabidopsis leaves expressing apoaequorin, a Ca(2+)-sensitive luminescent protein, in combination with a luminometer, to monitor [Ca(2+)](c) transients that occur in response to a variety of volatile compounds and to characterized the pharmacological properties of the increase in [Ca(2+)](c). When leaves were exposed to volatiles, [Ca(2+)](c) was transiently raised. The [Ca(2+)](c) increases induced by acyclic compounds were disrupted by Ruthenium Red, a potential plasma-membrane and endo-membrane Ca(2+)-permeable channel inhibitor, but not by 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA), an extracellular Ca(2+)-chelator, suggesting that acyclic compounds promote Ca(2+)-release from intracellular stores. On the other hand, the electrophilic compound (E)-2-hexenal promoted Ca(2+)-influx via ROS production by natural oxidation at the aquarius phase. In a gpa1-2 mutant lacking a canonical Galpha subunit, the [Ca(2+)](c) transients induced by all tested volatiles were not attenuated, suggesting that G-protein coupled receptors are not involved in the volatile-induced [Ca(2+)](c) transients in Arabidopsis leaves.
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