Saccharomyces cerevisiae-induced stomatal closure mainly mediated by salicylhydroxamic acid-sensitive peroxidases in Vicia faba

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• 作者：Jing Gao¹ ; Nan Wang¹ ; Gen-Xuan Wang ; ^{gwang@zju.edu.cn}
• 关键词：Ca2+ ; H2O2 ; NO ; Saccharomyces cerevisiae ; Water channels
• 刊名：Plant Physiology and Biochemistry
• 出版年：2013
• 出版时间：April, 2013
• 年：2013
• 卷：65
• 期：Complete
• 页码：27-31
• 全文大小：495 K

文摘

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 ¦Â-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 (Ca²⁺ antagonist) and EGTA (Ca²⁺ chelator) also impaired yeast-induced stomatal closure. Thus, it is concluded that H₂O₂, NO, water channels and Ca²⁺ are involved in yeast-induced stomatal closure.