Different signaling pathways involved during the suppression of stomatal opening by methyl jasmonate or abscisic acid

Abstract

The stomatal opening in abaxial epidermal strips of Nicotiana glauca is suppressed by the presence of abscisic acid (ABA) or methyl jasmonate (MJ). The role of calcium and related secondary messengers/signaling compounds during the restriction of stomatal opening by ABA or MJ was assessed. External calcium promoted, while EGTA prevented the process of stomatal closure, in case of both ABA and MJ. However, the effect of EGTA was more pronounced in the case of MJ than that of ABA. These observations established that the intracellular calcium is an important factor during stomatal closure induced not only by ABA but also by MJ. Lanthanum, verapamil, ruthenium red (Ca²⁺ channel blockers), trifluoperazine and W7 (calmodulin (CaM) antagonists) prevented MJ-induced stomatal closure but had only a partial effect on ABA-mediated stomatal closure. In contrast, U73122, 1-butanol (phospholipase C/D inhibitors) and phorbol myristate acetate (PMA, protein kinase C activator) reversed the stomatal closure caused by ABA but not that by MJ. Thus, the suppression of stomatal opening by ABA appears to be more dependent on phospholipases and protein kinase C than that by MJ. Similarly, the action of MJ on stomata seems to be crucially dependent on CaM and calcium channels of the guard cells. We suggest that MJ could be a useful tool, besides ABA, to analyze the sequence and pattern of signal transduction in stomatal guard cells.