Dual Role of Hydrogen Peroxide inArabidopsisGuard Cells in Response to Sulfur Dioxide

[摘要] Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death inArabidopsisleaves. High levels of SO2caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+antagonists EGTA and LaCl3blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2and[Ca2+]cytelevation. However, EGTA and LaCl3inhibited SO2-induced[Ca2+]cytincrease but did not suppress SO2-induced H2O2elevation. These results indicate that H2O2elevation triggered stomatal closure and cell death via[Ca2+]cytsignaling in SO2-stimulatedArabidopsisguard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2production plays critical role in SO2toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+signaling.

[学科分类] 药学