Abstract
BackgroundFusicoccin (FC), a fungal phytotoxin produced by Fusicoccum amygdale, causes the inhibition of ABA-induced stomatal closure. The mechanism of inhibition is remaining unclear. We analyzed the role of hydrogen peroxide (H2O2) and relationship between H2O2 removal and cytosolic pH changes during inhibition of ABA-induced stomatal closure by FC.ResultsAccording to the results, ABA treatment induced H2O2 production and stomatal closure, but FC inhibited the effects of ABA on these two parameters. Treatment with catalase (CAT) and NADPH oxidase inhibitor diphenylene iodonium (DPI) mimicked the effect of FC. These data suggest that inhibition of ABA effect by FC is related to the decrease of H2O2 levels in guard cells. Furthermore, similar to CAT, FC not only suppressed stomatal closure and H2O2 levels in guard cells treated with exogenous H2O2, but also reopened the stomata which had been closed by ABA and reduced the level of H2O2 that had been produced by ABA, indicating that FC causes H2O2 removal in guard cells. The butyric acid treatment simulated the effects of FC on the stomatal aperture and H2O2 levels in guard cells treated with exogenous H2O2 and had been closed by ABA, and both FC and butyric acid reduced cytosolic pH in guard cells of stomata treated with H2O2 and had been closed by ABA, which demonstrate that cytosolic acidification mediates FC-induced H2O2 removal.ConclusionThese results suggest that FC causes cytosolic acidification in guard cells, then induces H2O2 removal and reduces H2O2 levels in guard cells, finally inhibits stomatal closure induced by ABA.Electronic supplementary materialThe online version of this article (doi:10.1186/1999-3110-55-33) contains supplementary material, which is available to authorized users.
Highlights
Fusicoccin (FC), a fungal phytotoxin produced by Fusicoccum amygdale, causes the inhibition of Abscisic acid (ABA)-induced stomatal closure
We found that the inhibition of ABA-induced stomatal closure by FC involves a decrease in Hydrogen peroxide (H2O2) levels in guard cells of Vicia faba, and the decrease of H2O2 levels is mediated by cytosolic acidification
FC inhibits stomatal closure caused by ABA and reduces ABA-induced H2O2 levels in guard cells Previous studies have shown that FC, a fungal phytotoxin, causes irreversible stomatal opening (Assmann and Schwartz 1992; de Boer 1997)
Summary
Fusicoccin (FC), a fungal phytotoxin produced by Fusicoccum amygdale, causes the inhibition of ABA-induced stomatal closure. We analyzed the role of hydrogen peroxide (H2O2) and relationship between H2O2 removal and cytosolic pH changes during inhibition of ABA-induced stomatal closure by FC. Abscisic acid (ABA) is a phytohormone that plays vital roles in the control of growth and development and is involved in the response to various environmental stresses. It’s generally known ABA as a stress signal in plants. Drought and high salinity resulted in strong increases of plant ABA levels, accompanied by a major change in gene expression and in adaptive physiological responses (Christmann et al.2007; Rabbani et al 2003; Zeller et al 2009). ABA has been shown to induce stomatal closure and reduce the loss of transpirational water from plants under drought conditions (García-Mata and Lamattina 2001; Luan 2002). Phospholipid sphingosine-1-phosphate (SIP), phospholipase C and nitric oxide (NO) have been suggested to involve in ABA signaling pathways in stomatal closing movement (Hetherington 2001; Ng et al 2001; Bright et al 2006; Zhang et al 2007)
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