ABSTRACT
Chitosan (CHT) induces stomatal closure and thus plays a crucial role in plants to adapt to the adverse environments. Our previous results of a SA-deficient mutant nahG suggest that endogenous salicylic acid (SA) is involved in the CHT signaling in guard cells. Here in order to make the involvement definite, we examined stomatal responses to CHT of another SA-deficient mutant, sid2, and an SA receptor mutant, npr1-3. The sid2 mutation impaired CHT-induced stomatal closure and reactive oxygen species production and both impairments were complemented with exogenous SA application. Moreover, the CHT-induced stomatal closure is disrupted in the npr1-3 mutant. These results suggest that endogenous SA is involved in the CHT-induced stomatal closure via the SA receptor, NPR1.Abbreviations: SA: salicylic acid; ABA: abscisic acid; ROS: reactive oxygen species; NPR1: nonexpresser of pathogenesis-related genes1; CHT: chitosan; DAB: 3,3'-diaminobenzidine.
Subject(s)
Arabidopsis Proteins/metabolism , Arabidopsis/growth & development , Chitosan/pharmacology , Plant Stomata/drug effects , Salicylic Acid/pharmacology , Signal Transduction/drug effects , Abscisic Acid/metabolism , Arabidopsis/genetics , Arabidopsis Proteins/genetics , Chitosan/metabolism , Intramolecular Transferases/genetics , Mutation , Plant Growth Regulators/metabolism , Plant Stomata/growth & development , Plants, Genetically Modified , Reactive Oxygen Species/metabolism , Salicylic Acid/metabolism , Signal Transduction/geneticsABSTRACT
An elicitor chitosan (CHT) induces stomatal closure but the mechanism remains to be clarified. A phytohormone salicylic acid (SA) is crucial for elicitor-induced defense signaling in plants. Here we investigated whether endogenous SA is required for CHT signaling in guard cells. In the SA-deficient nahG mutant, treatment of CHT did not induce either apoplastic reactive oxygen species (ROS) production or stomatal closure but co-treatment of CHT and SA induced both apoplastic ROS production and stomatal closure, indicating the involvement of endogenous SA in CHT-induced apoplastic ROS production and CHT-induced stomatal closure. Furthermore, CHT induced transient cytosolic free calcium concentration increments in the nahG mutant in the presence of exogenous SA but not in the absence of exogenous SA. These results provide evidence that endogenous SA is a crucial element in CHT-induced stomatal closure.
Subject(s)
Arabidopsis/drug effects , Chitosan/pharmacology , Plant Growth Regulators/metabolism , Plant Stomata/drug effects , Salicylic Acid/metabolism , Signal Transduction , Abscisic Acid/metabolism , Arabidopsis/genetics , Arabidopsis/metabolism , Calcium/metabolism , Gene Expression , Mixed Function Oxygenases/deficiency , Mixed Function Oxygenases/genetics , Mutation , Plant Cells/drug effects , Plant Cells/metabolism , Plant Growth Regulators/pharmacology , Plant Stomata/genetics , Plant Stomata/metabolism , Salicylic Acid/pharmacologyABSTRACT
Gamma irradiation increased catalase activities at 0.1 kGy and decreased them at 10 kGy in Arabidopsis wild type and catalase-deficient mutants, cat3-1 and cat1 cat3. Irradiation induced DNA damage, H2O2 accumulation, and lipid peroxidation in both mutants as well as the wild type. Thus catalases might not be key enzymes protecting gamma irradiation-induced damage.
Subject(s)
Arabidopsis/enzymology , Arabidopsis/radiation effects , Catalase/metabolism , DNA Damage , Gamma Rays/adverse effects , Hydrogen Peroxide/metabolism , Lipid Peroxidation/radiation effects , Arabidopsis/genetics , Arabidopsis/metabolismABSTRACT
Salicylic acid (SA), yeast elicitor (YEL), and chitosan (CHT) induced stomatal closure in Arabidopsis wild-type and aba2-2 plants, induced stomatal closure in fluridon-treated wild-type plants, and induced stomatal closure in aos mutants. These results suggest that neither endogenous abscisic acid nor endogenous jasmonic acid is involved in SA-, YEL-, or CHT-induced stomatal closure.
