Cell death regulation but not abscisic acid signaling is required for enhanced immunity to Botrytis in Arabidopsis cuticle-permeable mutants
Cell death regulation but not abscisic acid signaling is required for enhanced immunity to Botrytis in Arabidopsis cuticle-permeable mutants
复制标题
在拟南芥角质层渗透性突变体中，增强对灰霉病的免疫力需要细胞死亡调节，而不是脱落酸信号传导
DOI：
10.1093/jxb/erz345
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发表时间：
2019-10-15
影响因子：
6.9
通讯作者：
Overmyer, Kirk
中科院分区：
文献类型：
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作者：
Cui, Fuqiang;Wu, Wenwu;Overmyer, Kirk
现有证据表明，在大多数但并非所有情况下，脱落酸（ABA）对真菌病原体灰葡萄孢的免疫有负面影响。ABA是角质层生物合成所必需的，而角质层通透性通过未知机制增强了对灰葡萄孢的免疫力。这种复杂的反应网络模糊了ABA在灰葡萄孢免疫中的作用。在此，我们研究了拟南芥ABA超敏感突变体蛋白磷酸酶2C四重突变体（pp2c - q）和对aba1增强反应突变体（era1 - 2）中ABA敏感性、角质层通透性和灰葡萄孢免疫之间的关系。pp2c - q和era1 - 2都没有表现出由ABA已知作用所预测的表型；相反，era1 - 2具有可渗透的角质层且对灰葡萄孢有抗性。我们在不同ABA敏感性的角质层可渗透突变体中进行了RNA - seq分析，并确定了一组核心的组成型激活基因，这些基因参与对灰葡萄孢的免疫以及对活体营养型病原体的易感性，且独立于ABA信号传导。此外，灰葡萄孢易感1（bos1）是一种细胞死亡失调且ABA敏感性增强的突变体，它抑制了角质层可渗透突变体对灰葡萄孢的免疫力，并且这种效应与bos1中伤口诱导的细胞死亡的扩散程度呈线性相关。总体而言，我们的数据表明，由角质层通透性赋予的对灰葡萄孢的免疫力可以在遗传上与PP2C调控的ABA敏感性解偶联，但需要对一个平行的ABA依赖的细胞死亡途径进行负调控。
Prevailing evidence indicates that abscisic acid (ABA) negatively influences immunity to the fungal pathogen Botrytis cinerea in most but not all cases. ABA is required for cuticle biosynthesis, and cuticle permeability enhances immunity to Botrytis via unknown mechanisms. This complex web of responses obscures the role of ABA in Botrytis immunity. Here, we addressed the relationships between ABA sensitivity, cuticle permeability, and Botrytis immunity in the Arabidopsis thaliana ABA-hypersensitive mutants protein phosphatase2c quadruple mutant (pp2c-q) and enhanced response to aba1 (era1-2). Neither pp2c-q nor era1-2 exhibited phenotypes predicted by the known roles of ABA; conversely, era1-2 had a permeable cuticle and was Botrytis resistant. We employed RNA-seq analysis in cuticle-permeable mutants of differing ABA sensitivities and identified a core set of constitutively activated genes involved in Botrytis immunity and susceptibility to biotrophs, independent of ABA signaling. Furthermore, botrytis susceptible1 (bos1), a mutant with deregulated cell death and enhanced ABA sensitivity, suppressed the Botrytis immunity of cuticle permeable mutants, and this effect was linearly correlated with the extent of spread of wound-induced cell death in bos1. Overall, our data demonstrate that Botrytis immunity conferred by cuticle permeability can be genetically uncoupled from PP2C-regulated ABA sensitivity, but requires negative regulation of a parallel ABA-dependent cell-death pathway.