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.
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
Arsenic causes physiological and structural disorders in plants. Proline is accumulated as a compatible solute in plants under various stress conditions and mitigates stresses. Here, we investigated the effects of exogenous proline on tobacco Bright Yellow-2 (BY-2) cultured cells under [Formula: see text] stress. Arsenate did not inhibit BY-2 cell growth at 40 and 50 μM but did it at 60 μM. Proline at 0.5 to 10 mM did not affect the cell growth but delayed it at 20 mM. At 40 μM [Formula: see text], neither 0.5 mM nor 1 mM proline affected the cell growth but 10 mM proline inhibited it. In the presence of [Formula: see text], 10 mM proline increased the number of Evans Blue-stained (dead) cells and decreased the number of total cells. Together, our results suggest that exogenous proline does not alleviate arsenate toxicity but enhances the sensitivity of BY-2 cells to arsenate.
Arsenic is toxic for plants. Our previous results showed that the application of proline enhanced the sensitivity of tobacco BY-2 cells to arsenate. In order to clarify the enhancement mechanism, we investigated the effects of other amino acids on the arsenate-stressed BY-2 cells. Glutamate at up to 10 mM did not affect the cell growth in the absence or presence of arsenate. Arginine at up to 10 mM did not affect the growth in the absence of arsenate but arginine at 10 mM enhanced the inhibition of the cell growth by arsenate. Alanine at up to 10 mM did not affect the cell growth under non-stressed condition but alanine at 10 mM significantly improved the cell growth under arsenate stress. These results suggest that alanine mitigates arsenate stress in BY-2 cells and that arginine like proline enhances the sensitivity of BY-2 cells to arsenate.
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