Arabidopsis local resistance to Botrytis cinerea involves salicylic acid and camalexin and requires EDS4 and PAD2, but not SID2, EDS5 or PAD4
Arabidopsis local resistance to Botrytis cinerea involves salicylic acid and camalexin and requires EDS4 and PAD2, but not SID2, EDS5 or PAD4
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DOI：
10.1046/j.1365-313x.2003.01794.x
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发表时间：
2003-07-01
期刊：
影响因子：
7.2
通讯作者：
Ausubel, FM
中科院分区：
文献类型：
--
作者：
Ferrari, S;Plotnikova, JM;Ausubel, FM
水杨酸（Salicylic acid，SA）是植物防御反应的重要调节因子，许多拟南芥突变体对细菌和真菌病原菌的抗性受损，表现出SA积累、感知或信号转导的缺陷。然而，SA依赖的防御反应对坏死性真菌的作用目前还不清楚。我们确定了一组先前确定的拟南芥突变体的敏感性受损的防御反应，坏死营养型真菌病原体灰葡萄孢。B的发育速度。在初次感染的叶片上的灰霉病症状受到由基因EIN 2、JAR 1、EDS 4、PAD 2和PAD 3介导的应答的影响，但在很大程度上独立于EDS 5、SID 2/ICS 1和PAD 4。此外，表达nahG转基因或用苯丙氨酸解氨酶（PAL）抑制剂处理的植物表现出增强的症状，表明SA通过PAL合成，而不是通过异分支酸合酶（ICS），介导病变发展。此外，病变发展的程度与防御素或PR 1表达无关，尽管它部分依赖于Camalexin积累。虽然npr 1突变体叶片通常对B敏感。cinerea感染时，双ein 2 npr 1突变体比ein 2植株更敏感，外源SA的施用降低了B。通过NPR 1依赖的机制，可以模仿cpr 1突变的灰斑病变的大小。这些数据表明，局部耐B。灰霉病需要乙烯、茉莉酸和SA介导的信号传导，影响这种抗性的SA不需要ICS 1，并且可能通过PAL合成，并且camalexin限制病变发展。
Salicylic acid (SA) is an important regulator of plant defense responses, and a variety of Arabidopsis mutants impaired in resistance against bacterial and fungal pathogens show defects in SA accumulation, perception, or signal transduction. Nevertheless, the role of SA-dependent defense responses against necrotrophic fungi is currently unclear. We determined the susceptibility of a set of previously identified Arabidopsis mutants impaired in defense responses to the necrotrophic fungal pathogen Botrytis cinerea . The rate of development of B. cinerea disease symptoms on primary infected leaves was affected by responses mediated by the genes EIN2, JAR1, EDS4, PAD2, and PAD3, but was largely independent of EDS5, SID2 /ICS1, and PAD4 . Furthermore, plants expressing a nahG transgene or treated with a phenylalanine ammonia lyase (PAL) inhibitor showed enhanced symptoms, suggesting that SA synthesized via PAL, and not via isochorismate synthase (ICS), mediates lesion development. In addition, the degree of lesion development did not correlate with defensin or PR1 expression, although it was partially dependent upon camalexin accumulation. Although npr1 mutant leaves were normally susceptible to B. cinerea infection, a double ein2 npr1 mutant was significantly more susceptible than ein2 plants, and exogenous application of SA decreased B. cinerea lesion size through an NPR1-dependent mechanism that could be mimicked by the cpr1 mutation. These data indicate that local resistance to B. cinerea requires ethylene-, jasmonate-, and SA-mediated signaling, that the SA affecting this resistance does not require ICS1 and is likely synthesized via PAL, and that camalexin limits lesion development.