Inhibition of ABA-induced stomatal closure by fusicoccin is associated with cytosolic acidification-mediated hydrogen peroxide removal

BACKGROUND: Fusicoccin (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 (H(2)O(2)) and relationship between H(2)O(2) removal and cytosolic pH changes during inhibition of ABA-induced stomatal closure by FC. RESULTS: According to the results, ABA treatment induced H(2)O(2) 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 H(2)O(2) levels in guard cells. Furthermore, similar to CAT, FC not only suppressed stomatal closure and H(2)O(2) levels in guard cells treated with exogenous H(2)O(2), but also reopened the stomata which had been closed by ABA and reduced the level of H(2)O(2) that had been produced by ABA, indicating that FC causes H(2)O(2) removal in guard cells. The butyric acid treatment simulated the effects of FC on the stomatal aperture and H(2)O(2) levels in guard cells treated with exogenous H(2)O(2) and had been closed by ABA, and both FC and butyric acid reduced cytosolic pH in guard cells of stomata treated with H(2)O(2) and had been closed by ABA, which demonstrate that cytosolic acidification mediates FC-induced H(2)O(2) removal. CONCLUSION: These results suggest that FC causes cytosolic acidification in guard cells, then induces H(2)O(2) removal and reduces H(2)O(2) levels in guard cells, finally inhibits stomatal closure induced by ABA. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1999-3110-55-33) contains supplementary material, which is available to authorized users.