Rao M V, Lee H, Creelman R A, Mullet J E, Davis K R
Plant Biotechnology Center, Ohio State University, Columbus, Ohio 43210, USA.
Plant Cell. 2000 Sep;12(9):1633-46. doi: 10.1105/tpc.12.9.1633.
Recent studies suggest that cross-talk between salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene-dependent signaling pathways regulates plant responses to both abiotic and biotic stress factors. Earlier studies demonstrated that ozone (O(3)) exposure activates a hypersensitive response (HR)-like cell death pathway in the Arabidopsis ecotype Cvi-0. We now have confirmed the role of SA and JA signaling in influencing O(3)-induced cell death. Expression of salicylate hydroxylase (NahG) in Cvi-0 reduced O(3)-induced cell death. Methyl jasmonate (Me-JA) pretreatment of Cvi-0 decreased O(3)-induced H(2)O(2) content and SA concentrations and completely abolished O(3)-induced cell death. Cvi-0 synthesized as much JA as did Col-0 in response to O(3) exposure but exhibited much less sensitivity to exogenous Me-JA. Analyses of the responses to O(3) of the JA-signaling mutants jar1 and fad3/7/8 also demonstrated an antagonistic relationship between JA- and SA-signaling pathways in controlling the magnitude of O(3)-induced HR-like cell death.
近期研究表明，水杨酸（SA）、茉莉酸（JA）和乙烯依赖的信号通路之间的相互作用调节着植物对非生物和生物胁迫因子的响应。早期研究表明，暴露于臭氧（O₃）会激活拟南芥生态型Cvi-0中类似过敏反应（HR）的细胞死亡途径。我们现在已经证实了SA和JA信号在影响O₃诱导的细胞死亡中的作用。水杨酸羟化酶（NahG）在Cvi-0中的表达减少了O₃诱导的细胞死亡。用茉莉酸甲酯（Me-JA）预处理Cvi-0可降低O₃诱导的H₂O₂含量和SA浓度，并完全消除O₃诱导的细胞死亡。Cvi-0在暴露于O₃时合成的JA与Col-0一样多，但对外源Me-JA的敏感性要低得多。对JA信号突变体jar1和fad3/7/8对O₃的反应分析也表明，在控制O₃诱导的类似HR的细胞死亡程度方面，JA和SA信号通路之间存在拮抗关系。
