Signaling pathways that regulate the enhanced disease resistance of Arabidopsis "defense, no death" mutants.
Signaling pathways that regulate the enhanced disease resistance of Arabidopsis "defense, no death" mutants.
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DOI：
10.1094/mpmi-21-10-1285
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发表时间：
2008-10
期刊：
影响因子：
--
通讯作者：
Bent AF
中科院分区：
文献类型：
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作者：
Genger RK;Jurkowski GI;McDowell JM;Lu H;Jung HW;Greenberg JT;Bent AF
拟南芥dnd 1和dnd 2突变体缺乏环核苷酸门控离子通道蛋白，并进行avr/R介导的防御，大大降低了过敏反应（HR）。它们还表现出提高的广谱抗病性和组成性升高的水杨酸（SA）水平。我们检测了NPR 1、SID 2（EDS 16）、NDR 1和EIN 2对dnd表型的贡献。影响SA积累或信号传导的突变（npr 2，npr 1和ndr 1）消除了dnd突变体对假单胞菌pv.番茄和寄生透明霜霉而不是灰葡萄孢。当SA相关通路被破坏时，NPR 1依赖性和NPR 1非依赖性/SA依赖性通路的组成性激活被重定向到PDF1.2相关通路。这种PDF1.2过表达在丁香假单胞菌感染后被下调。乙烯信号的中断取消了增强的抗性B。cinerea，而不是P. degeniae和H.寄生虫。然而，NPR 1、SID 2、NDR 1或EIN 2的缺失并没有可检测地改变dnd突变体中降低的HR。dnd ein 2植物对B的敏感性。灰霉病菌尽管其HR表型降低，但表明细胞死亡抑制不是对坏死营养型病原体的dnd抗性的主要原因。对B抗性的部分恢复。在dnd 1 npr 1 ein 2三重突变体中的灰霉病表明这种抗性不完全是EIN 2依赖性的。上述发现表明，dnd突变体的广谱抗性是由于多种防御途径的激活和/或敏化而发生的，然而所研究的途径中没有一种是降低HR表型所需的。
Arabidopsis dnd1 and dnd2 mutants lack cyclic nucleotide-gated ion channel proteins and carry out avr/R-mediated defense with a greatly reduced hypersensitive response (HR). They also exhibit elevated broad-spectrum disease resistance and constitutively elevated salicylic acid (SA) levels. We examined the contributions of NPR1, SID2 (EDS16), NDR1 and EIN2 to dnd phenotypes. Mutations that affect SA accumulation or signaling (sid2, npr1 and ndr1) abolished the enhanced resistance of dnd mutants against Pseudomonas syringae pv. tomato and Hyaloperonospora parasitica but not Botrytis cinerea. When SA-associated pathways were disrupted, the constitutive activation of NPR1-dependent and NPR1-independent/SA-dependent pathways was redirected toward PDF1.2-associated pathways. This PDF1.2 over-expression was down-regulated after infection by P. syringae. Disruption of ethylene signaling abolished the enhanced resistance to B. cinerea but not P. syringae or H. parasitica. However, loss of NPR1, SID2, NDR1 or EIN2 did not detectably alter the reduced HR in dnd mutants. The susceptibility of dnd ein2 plants to B. cinerea despite their reduced-HR phenotype suggests that cell death repression is not the primary cause of dnd resistance to necrotrophic pathogens. The partial restoration of resistance to B. cinerea in dnd1 npr1 ein2 triple mutants indicated that this resistance is not entirely EIN2-dependent. The above findings indicate that the broad spectrum resistance of dnd mutants occurs due to activation and/or sensitization of multiple defense pathways, yet none of the investigated pathways are required for the reduced-HR phenotype.