Low Oleic Acid-Derived Repression of Jasmonic Acid-Inducible Defense Responses Requires the WRKY50 and WRKY51 Proteins
Low Oleic Acid-Derived Repression of Jasmonic Acid-Inducible Defense Responses Requires the WRKY50 and WRKY51 Proteins
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DOI：
10.1104/pp.110.166876
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发表时间：
2011-01-01
期刊：
影响因子：
7.4
通讯作者：
Kachroo, Aardra
中科院分区：
文献类型：
--
作者：
Gao, Qing-Ming;Venugopal, Srivathsa;Kachroo, Aardra
油酸（18：1）水平降低后诱导的信号传导同时上调水杨酸（SA）介导的反应，并抑制茉莉酸（JA）诱导的防御，导致对生物营养型的抗性增强，但对坏死营养型的易感性增加。SA和信号组分增强的疾病易感性1在这种低18：1衍生的途径中冗余地起作用以诱导SA信号传导，但在JA反应的抑制中不起作用。我们发现，在低-18：1条件下，JA介导的信号转导的抑制是通过WRKY 50和WRKY 51蛋白介导的。WRKY 50和WRKY 51的敲除突变降低了SA水平，但没有恢复发病机制相关的基因表达或病原体抗性的基础水平，在低18：1含拟南芥（拟南芥）突变体，抑制SA不敏感2（ssi 2）。与此相反，两个JA诱导的PDF1.2（防御素）的表达和基础抗灰葡萄孢恢复。同时在两个WRKY基因突变（ssi 2 wrky 50 wrky 51）没有进一步增强JA或葡萄孢相关的反应。与ssi 2植物相同，ssi 2 wrky 50和ssi 2 wrky 51植物含有高水平的活性氧，并表现出增强的细胞死亡。这表明，高活性氧水平或增加细胞死亡是不负责的增强敏感性的ssi 2植物B。灰绿色外源SA抑制野生型中JA诱导的PDF1.2表达，但不抑制wrky 50或wrky 51突变体植物中的表达。这些结果表明，WRKY 50和WRKY 51蛋白介导SA和低18：1依赖的JA信号转导抑制。
Signaling induced upon a reduction in oleic acid (18: 1) levels simultaneously up-regulates salicylic acid (SA)-mediated responses and inhibits jasmonic acid (JA)-inducible defenses, resulting in enhanced resistance to biotrophs but increased susceptibility to necrotrophs. SA and the signaling component Enhanced Disease Susceptibility1 function redundantly in this low-18:1-derived pathway to induce SA signaling but do not function in the repression of JA responses. We show that repression of JA-mediated signaling under low-18: 1 conditions is mediated via the WRKY50 and WRKY51 proteins. Knockout mutations in WRKY50 and WRKY51 lowered SA levels but did not restore pathogenesis-related gene expression or pathogen resistance to basal levels in the low-18: 1-containing Arabidopsis (Arabidopsis thaliana) mutant, suppressor of SA insensitivity2 (ssi2). In contrast, both JA-inducible PDF1.2 (defensin) expression and basal resistance to Botrytis cinerea were restored. Simultaneous mutations in both WRKY genes (ssi2 wrky50 wrky51) did not further enhance the JA or Botrytis-related responses. The ssi2 wrky50 and ssi2 wrky51 plants contained high levels of reactive oxygen species and exhibited enhanced cell death, the same as ssi2 plants. This suggested that high reactive oxygen species levels or increased cell death were not responsible for the enhanced susceptibility of ssi2 plants to B. cinerea. Exogenous SA inhibited JA-inducible PDF1.2 expression in the wild type but not in wrky50 or wrky51 mutant plants. These results show that the WRKY50 and WRKY51 proteins mediate both SA-and low-18:1-dependent repression of JA signaling.