Involvement of salicylate and jasmonate signaling pathways in Arabidopsis interaction with Fusarium graminearum.

Involvement of salicylate and jasmonate signaling pathways in Arabidopsis interaction with Fusarium graminearum.
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DOI:
10.1094/mpmi-23-7-0861
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发表时间:
2010-07
期刊:
Molecular plant-microbe interactions : MPMI
影响因子:
--
通讯作者:
Shah J
Shah J
中科院分区:
其他
文献类型:
--
作者:
Makandar R;Nalam V;Chaturvedi R;Jeannotte R;Sparks AA;Shah J

文献摘要

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禾谷镰刀菌(Fusarium graminearum)是小麦和大麦赤霉病(Fusarium head blight,FHB)的主要病原。这种真菌也可以在拟南芥中定植。在组成型过表达PR基因非表达子1(NPR 1)基因的转基因小麦和拟南芥植物中增强了抗病性,所述NPR 1基因调节水杨酸(SA)信号传导并调节茉莉酸(JA)依赖性防御的激活。在这里,我们提供了一些证据,揭示了SA和JA信号在拟南芥防御F。禾谷早熟禾SA水平在真菌接种的叶片和SA的应用和生物激活的系统获得的抗性增强的抗性。此外,SA的积累和信号转导的中断,在npr2突变体和NahG转基因植物,和npr1和wrky18突变体,分别导致提高这种真菌在叶片和花序的易感性。JA信号与SA信号在受真菌攻击的植物中平行激活。但是,JA途径突变体opr3、coi1和jar1的超抗性表明该途径有助于易感性。遗传和生化实验表明,JA途径通过减弱SA信号在真菌接种植物中的激活来促进疾病。然而,与npr1突变体相比,jar1 npr1双突变体的超易感性表明JAR1也有助于防御,这意味着JA和JAR1依赖机制在这种相互作用中的二分法作用。
Fusarium graminearum is the principal causative agent of Fusarium head blight (FHB), a devastating disease of wheat and barley. This fungus can also colonize Arabidopsis thaliana. Disease resistance was enhanced in transgenic wheat and Arabidopsis plants that constitutively over-express the NONEXPRESSOR OF PR GENES 1 (NPR1) gene, which regulates salicylic acid (SA) signaling and modulates the activation of jasmonic acid (JA)-dependent defenses. Here, we provide several lines of evidence that reveal an important role for SA and JA signaling in Arabidopsis defense against F. graminearum. SA level was elevated in fungus-inoculated leaves and SA application and biologically activated systemic acquired resistance enhanced resistance. Furthermore, the disruption of SA accumulation and signaling in the sid2 mutant and NahG transgenic plant, and the npr1 and wrky18 mutants, respectively, resulted in heightened susceptibility to this fungus in leaves and inflorescence. JA signaling was activated in parallel with SA signaling in the fungus-challenged plants. But, the hyper-resistance of the JA pathway mutants, opr3, coi1 and jar1 indicates that this pathway contributes to susceptibility. Genetic and biochemical experiments indicate that the JA pathway promotes disease by attenuating the activation of SA signaling in fungus-inoculated plants. However, the hyper-susceptibility of the jar1 npr1 double mutant compared to the npr1 mutant suggests that JAR1 also contributes to defense, signifying a dichotomous role of JA and JAR1-dependent mechanism in this interaction.