Saccharomyces cerevisiae induced stomatal closure in a dose-dependent manner on Vicia faba L. (cv. Daqingpi). Using pharmacological inhibitors in this study, we found that stomatal closure was completely inhibited by salicylhydroxamic acid (SHAM) and reduced glutathione (GSH), whereas slightly inhibited by diphenyleneiodonium chloride (DPI), suggesting that H2O2 was mostly produced by cell wall peroxidases. The specific NO scavenger (cPTIO), NO synthase (NOS) inhibitor NG-nitro-l-arginine methyl ester (l-NAME) and sodium azide (NaN3; inhibitor of nitrate reductase) prevented yeast-induced stomatal closure, suggesting that NO in guard cells of V. faba is derived from both NOS-like enzyme and nitrate reductase. Results of HgCl2 and β-mercaptoethanol (ME) treatment (as a functional inhibitor of water channels and its reversing agent, respectively) suggest that water channels are involved in yeast-induced stomatal movements. CoCl2 (the blocker of calcium channel), LaCl3 (Ca(2+) antagonist) and EGTA (Ca(2+) chelator) also impaired yeast-induced stomatal closure. Thus, it is concluded that H2O2, NO, water channels and Ca(2+) are involved in yeast-induced stomatal closure.
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